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Роль воспалительного старения в развитии хронической сердечной недостаточности и остеопороза: обзор литературы
Роль воспалительного старения в развитии хронической сердечной недостаточности и остеопороза: обзор литературы
Ларина В.Н., Щербина Е.С. Роль воспалительного старения в развитии хронической сердечной недостаточности и остеопороза: обзор литературы // CardioСоматика. 2024. Т. 15, № 3. С. 231–242.
DOI: https://doi.org/10.17816/CS632927
DOI: https://doi.org/10.17816/CS632927
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Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Проблема взаимосвязи хронической сердечной недостаточности (ХСН) и остеопороза у мультиморбидного пациента актуальна в свете старения населения. Концепция «inflammaging» (воспалительного старения) позволяет рассматривать продолжительный процесс субклинического воспаления как адаптацию. В зависимости от положительного или отрицательного влияния этого фактора на организм человека результатом может быть здоровое долголетие или старение, сопровождающееся гериатрическими синдромами и возникновением различных патологий, включая развитие ХСН и остеопороза. В данной статье освещена проблема воспалительного старения как системного фактора в контексте развития ХСН и остеопороза: обсуждается функция воспалительных маркеров, а также роль инфламмасомы NLRP3 в иммуновоспалительном пути развития как ХСН, так и остеопороза посредством влияния на формирование провоспалительных цитокинов. Рассматриваются способы влияния на различные звенья патогенеза, что может лежать в основе разработки новых методов терапии.
Ключевые слова: сердечная недостаточность, остеопороз, воспалительное старение
Keywords: heart failure. osteoporosis, inflammaging
Ключевые слова: сердечная недостаточность, остеопороз, воспалительное старение
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Keywords: heart failure. osteoporosis, inflammaging
Полный текст
Список литературы
1. Overview of Ageing. В: World Health Organization [Internet]. Режим доступа: https://www.who.int/ru/health-topics/ageing#tab=tab_1 Дата обращения: 23.02.2024.
2. Decade of healthy ageing: baseline report, 2021. В: World Health Organization [Internet]. Режим доступа: https://www.who.int/publicationsMem/9789240017900 Дата обращения: 23.02.2024.
3. Franceschi C., Bonafe M., Valensin S., et al. Inflamm-aging. An evolutionary perspective on immunosenescence // Ann N Y Acad Sci. 2000. Vol. 908. Р. 208–218.
doi: 10.1111/j.1749-6632.2000.tb06651.x
4. Savarese G., Becher P.M., Lund L.H., et al. Global burden of heart failure: a comprehensive and updated review of epidemiology // Cardiovasc Res. 2023. Vol. 118, N. 17.
Р. 3272–3287. doi: 10.1093/cvr/cvac013
5. Артемьева О.В., Ганковская Л.В. Воспалительное старение как основа возраст-ассоциированной патологии // Медицинская иммунология. 2020. Т. 22, № 3.
С. 419–432. doi: 10.15789/1563-0625-IAT-1938.
6. Артемьева О.В., Греченко В.В., Громова Т.В., и др. Синдром старческой астении: неоднозначная роль воспалительного старения // Иммунология. 2022. Т. 43, № 6.
С. 746–756. doi: 10.33029/0206-4952-2022-43-6-746-756
7. Montecino-Rodriguez E., Berent-Maoz B., Dorshkind K. Causes, consequences, and reversal of immune system aging // J Clin Invest. 2013. Vol. 123, N. 3. Р. 958–965.
doi: 10.1172/JCI64096
8. Bai L., Liu Y., Zhang X., et al. Osteoporosis remission via an anti-inflammaging effect by icariin activated autophagy // Biomaterials. 2023. Vol. 297. Р. 122–125.
doi: 10.1016/j.biomaterials.2023.122125
9. DeBerge M., Shah S.J., Wilsbacher L., et al. Macrophages in heart failure with reduced versus preserved ejection fraction // Trends Mol Med. 2019. Vol. 25, N. 4. Р. 328–340.
doi: 10.1016/j.molmed.2019.01.002
10. Mizushima N., Komatsu M. Autophagy: renovation of cells and tissues // Cell. 2011. Vol. 147, N. 4. Р. 728–741. doi: 10.1016/j.cell.2011.10.026
11. Chatterjee N., Walker G.C. Mechanisms of DNA damage, repair, and mutagenesis // Environ Mol Mutagen. 2017. Vol. 58, N. 5. Р. 235–263. doi: 10.1002/em.22087
12. Mezzaroma E., Toldo S., Farkas D., et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse // Proc Natl Acad Sci USA. 2011. Vol. 108, N. 49. Р. 19725–19730. doi: 10.1073/pnas.1108586108
13. Hulsmans M., Sager H.B., Roh J.D., et al. Cardiac macrophages promote diastolic dysfunction // J Exp Med. 2018. Vol. 215, N. 2. Р. 423–440. doi: 10.1084/jem.20171274
14. Liang Z., Zhang T., Liu H., et al. Inflammaging: The ground for sarcopenia? // Exp Gerontol. 2022. Vol. 68. Р. 111931. doi: 10.1016/j.exger.2022.111931
15. Antuña E., Cachán-Vega C., Bermejo-Millo J.C., et al. Inflammaging: Implications in Sarcopenia // Int J Mol Sci. 2022. Vol. 23, N. 23. Р. 15039. doi: 10.3390/ijms232315039
16. Ajoolabady A., Pratico D., Vinciguerra M., et al. Inflammaging: mechanisms and role in the cardiac and vasculature // Trends Endocrinol Metab. 2023. Vol. 34, N. 6. Р. 373–387.
doi: 10.1016/j.tem.2023.03.005
17. Казанова П.В., Басиева М.А., Шварц В.А. Иммунное ремоделирование в патогенезе фибрилляции предсердий // Анналы аритмологии. 2023. Т. 20, № 2. С. 119–130.
doi: 10.15275/annaritmol.2023.2.7
18. Yao Y., Yang M., Liu D., et al. Immune remodeling and atrial fibrillation // Front Physiol. 2022. Vol. 13. Р. 927221. doi: 10.3389/fphys.2022.927221
19. Ионин В.А., Барашкова Е.И., Заславская Е.Л., и др. Биомаркеры воспаления, параметры, характеризующие ожирение и ремоделирование сердца, у пациентов с фибрилляцией предсердий и метаболическим синдромом // Российский кардиологический журнал. 2021. Т. 26, № 3. С. 4343. doi: 10.15829/15604071-2021-4343
20. Santhanakrishnan R., Chong J.P., Ng T.P., et al. Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction // Eur J Heart Fail. 2012. Vol. 14, N. 12. Р. 1338–1347. doi: 10.1093/eurjhf/hfs130
21. Алиева А.М., Резник Е.В., Пинчук Т.В., и др. Фактор дифференцировки роста — 15 (GDF-15) как биологический маркер при сердечной недостаточности // Архивъ внутренней медицины. 2023. Т. 13, № 1. С. 14–23. doi: 10.20514/2226-6704-2023-13-1-14-23
22. Bouabdallaoui N., Claggett B., Zile M.R., et al. Growth differentiation factor-15 is not modified by sacubitril/valsartan and is an independent marker of risk in patients with heart failure and reduced ejection fraction: the PARADIGM-HF trial // Eur J Heart Fail. 2018. Vol. 20, N. 12. Р. 1701–1709. doi: 10.1002/ejhf.1301
23. Витт К.Н., Кужелева Е.А., Тукиш О.В., и др. Низкоинтенсивное воспаление как проявление коморбидности и фактор неблагоприятного клинического течения сердечной недостаточности с сохранённой фракцией выброса // Кардиоваскулярная терапия и профилактика. 2024. Т. 23, № 2. С. 3847. doi: 10.15829/1728-8800-2024-3847
24. Ballak D.B., Stienstra R., Tack C.J., et al. IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance // Cytokine. 2015. Vol. 75, N. 2. Р. 280–290. doi: 10.1016/j.cyto.2015.05.005
25. Reilly S.M., Saltiel A.R. Adapting to obesity with adipose tissue inflammation // Nat Rev Endocrinol. 2017. Vol. 13, N. 11. Р. 633–643. doi: 10.1038/nrendo.2017.90
26. Gao J., Xie Q., Wei T., et al. Nebivolol Improves Obesity-Induced Vascular Remodeling by Suppressing NLRP3 Activation // J Cardiovasc Pharmacol. 2019. Vol. 73, N. 5.
Р. 326–333. doi: 10.1097/FJC.0000000000000667
27. Белая Ж.Е., Белова К.Ю., Бирюкова Е.В., и др. Федеральные клинические рекомендации по диагностике, лечению и профилактике остеопороза // Остеопороз и остеопатии. 2021. Т. 24, № 2. С. 4–47. doi: 10.14341/osteo1293
28. Curtis E., Litwic A., Cooper C., et al. Determinants of Muscle and Bone Aging // J Cell Physiol. 2015. Vol. 230, N. 11. Р. 2618–2625. doi: 10.1002/jcp.25001
29. Lloyd B.D., Williamson D.A., Singh N.A., et al. Recurrent and injurious falls in the year following hip fracture: a prospective study of incidence and risk factors from the Sarcopenia and Hip Fracture study // J Gerontol A Biol Sci Med Sci. 2009. Vol. 64, N. 5. Р. 599–609. doi: 10.1093/gerona/glp003
30. Pajarinen J., Lin T., Gibon E., et al. Mesenchymal stem cell-macrophage crosstalk and bone healing // Biomaterials. 2019. Vol. 196. Р. 80–89. doi: 10.1016/j.biomaterials.2017.12.025
31. Raggatt L.J., Wullschleger M.E., Alexander K.A., et al. Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification // Am J Pathol. 2014. Vol. 184, N. 12. Р. 3192–3204. doi: 10.1016/j.ajpath.2014.08.017
32. Sebastián C., Herrero C., Serra M., et al. Telomere shortening and oxidative stress in aged macrophages results in impaired STAT5a phosphorylation // J Immunol. 2009. Vol. 183,
N. 4. Р. 2356–2364. doi: 10.4049/jimmunol.0901131
33. Vi L., Baht G.S., Soderblom E.J., et al. Macrophage cells secrete factors including LRP1 that orchestrate the rejuvenation of bone repair in mice // Nat Commun. 2018. Vol. 9, N. 1.
Р. 5191. doi: 10.1038/s41467-018-07666-0
34. Saul D., Khosla S. Fracture healing in the setting of endocrine diseases, aging, and cellular senescence // Endocr Rev. 2022. Vol. 43, N. 6. Р. 984–1002. doi: 10.1210/endrev/bnac008
35. Тополянская С.В. Роль интерлейкина 6 при старении и возрастассоциированных заболеваниях // Клиницист. 2020. Т. 14, № 3–4. С. К633.
doi: 10.17650/1818-8338-2020-14-3-4-К633
36. Ballesteros J., Rivas D., Duque G. The role of the kynurenine pathway in the pathophysiology of frailty, sarcopenia, and osteoporosis // Nutrients. 2023. Vol. 15, N. 14. Р. 3132.
doi: 10.3390/nu15143132
37. Ge Y., Huang M., Yao Y.M. Recent advances in the biology of IL-1 family cytokines and their potential roles in development of sepsis // Cytokine Growth F R. 2019. Vol. 45. Р. 24–34. doi: 10.1016/j.cytogfr.2018.12.004
38. Jiang N., An J., Yang K., et al. NLRP3 inflammasome: A new target for prevention and control of osteoporosis? // Front Endocrinol (Lausanne). 2021. Vol. 12. Р. 752546.
doi: 10.3389/fendo.2021.752546
39. Fischer J., Hans D., Lamy O., et al. "Inflammaging" and bone in the OsteoLaus cohort // Immun Ageing. 2020. Vol. 17. Р. 5. doi: 10.1186/s12979-020-00177-x
40. Zhu Y., Tchkonia T., Pirtskhalava T., et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs // Aging Cell. 2015. Vol. 14, N. 4. Р. 644–658.
doi: 10.1111/acel.12344
41. Моргунова Г.В., Хохлов А.Н. Препараты с сенолитической активностью: перспективы и возможные ограничения // Вестник Московского университета. Серия 16. Биология. 2023. Т. 78, № 4. С. 278–284. doi: 10.55959/MSU0137-0952-16-78-4-3
42. Toldo S., Mezzaroma E., Buckley L.F., et al. Targeting the NLRP3 inflammasome in cardiovascular diseases // Pharmacol Ther. 2022. Vol. 236. Р. 108053.
doi: 10.1016/j.pharmthera.2021.108053
43. Solomon S.D., McMurray J.J.V., Anand I.S., et al. Investigators and committees. angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction // N Engl J Med. 2019. Vol. 381, N. 17. Р. 1609–1620. doi: 10.1056/NEJMoa1908655
44. Compston J.E., McClung M.R., Leslie W.D. Osteoporosis // Lancet. 2019. Vol. 393, N. 10169. Р. 364–376. doi: 10.1016/S0140-6736(18)32112-3
2. Decade of healthy ageing: baseline report, 2021. In: World Health Organization [Internet]. Available from: https://www.who.int/publicationsMem/9789240017900 Accessed: 23.02.2024.
3. Franceschi C, Bonafe M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:208–218.
doi: 10.1111/j.1749-6632.2000.tb06651.x
4. Savarese G, Becher PM, Lund LH, et al. Global burden of heart failure: a comprehensive and updated review of epidemiology. Cardiovasc Res. 2023;118(17):3272–3287.
doi: 10.1093/cvr/cvac013
5. Artemyeva OV, Gankovskaya LV, Inflammagingas the basis of age-associated diseases. Meditsinskaya Immunologiya. 2020;22(3):419–432. doi: 10.15789/1563-0625-IAT-1938
6. Artemyeva OV, Grechenko VV, Gromova TV, et al. Frailty: a controversial role of inflammaging. Immunologiya. 2022;43(6):746–56. doi: 10.33029/0206-4952-2022-43-6-746-756
7. Montecino-Rodriguez E, Berent-Maoz B, Dorshkind K. Causes, consequences, and reversal of immune system aging. J Clin Invest. 2013;123(3):958–965. doi: 10.1172/JCI64096
8. Bai L, Liu Y, Zhang X, et al. Osteoporosis remission via an anti-inflammaging effect by icariin activated autophagy. Biomaterials. 2023;297:122–125.
doi: 10.1016/j.biomaterials.2023.122125
9. DeBerge M, Shah SJ, Wilsbacher L, et al. Macrophages in heart failure with reduced versus preserved ejection fraction. Trends Mol Med. 2019;25(4):328–340.
doi: 10.1016/j.molmed.2019.01.002
10. Mizushima N, Komatsu M. Autophagy: renovation of cells and tissues. Cell. 2011;147(4):728–741. doi: 10.1016/j.cell.2011.10.026
11. Chatterjee N, Walker GC. Mechanisms of DNA damage, repair, and mutagenesis. Environ Mol Mutagen. 2017;58(5):235–263. doi: 10.1002/em.22087
12. Mezzaroma E, Toldo S, Farkas D, et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse. Proc Natl Acad Sci USA. 2011;108(49):19725–19730. doi: 10.1073/pnas.1108586108
13. Hulsmans M, Sager HB, Roh JD, et al. Cardiac macrophages promote diastolic dysfunction. J Exp Med. 2018;215(2):423–440. doi: 10.1084/jem.20171274
14. Liang Z, Zhang T, Liu H, et al. Inflammaging: The ground for sarcopenia? Exp Gerontol. 2022;68:111931. doi: 10.1016/j.exger.2022.111931
15. Antuña E, Cachán-Vega C, Bermejo-Millo JC, et al. Inflammaging: Implications in Sarcopenia. Int J Mol Sci. 2022;23(23):15039. doi: 10.3390/ijms232315039
16. Ajoolabady A, Pratico D, Vinciguerra M, et al. Inflammaging: mechanisms and role in the cardiac and vasculature. Trends Endocrinol Metab. 2023;34(6):373–387.
doi: 10.1016/j.tem.2023.03.005
17. Kazanova PV, Basieva MA, Shvartz VA. Immune remodeling in the pathogenesis of atrial fibrillation. Annaly aritmologii. 2023;20(2):119–130. doi: 10.15275/annaritmol.2023.2.7
18. Yao Y, Yang M, Liu D, et al. Immune remodeling and atrial fibrillation. Front Physiol. 2022;13:927221. doi: 10.3389/fphys.2022.927221
19. Ionin VA, Barashkova EI, Zaslavskaya EL, et al. Biomarkers of inflammation, parameters characterizing obesity and cardiac remodeling in patients with atrial fibrillation and metabolic syndrome. Russian Journal of Cardiology. 2021;26(3):4343. doi: 10.15829/15604071-2021-4343
20. Santhanakrishnan R, Chong JP, Ng TP, et al. Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction. Eur J Heart Fail. 2012;14(12):1338–1347. doi: 10.1093/eurjhf/hfs130
21. Alieva AM, Reznik EV, Pinchuk TV, et al. Growth Differentiation Factor-15 (GDF-15) is a Biological Marker in Heart Failure. The Russian Archives of Internal Medicine.
2023;13(1):14–23. doi: 10.20514/2226-6704-2023-13-1-14-23
22. Bouabdallaoui N, Claggett B, Zile MR, et al. Growth differentiation factor-15 is not modified by sacubitril/valsartan and is an independent marker of risk in patients with heart failure and reduced ejection fraction: the PARADIGM-HF trial. Eur J Heart Fail. 2018;20(12):1701–1709. doi: 10.1002/ejhf.1301
23. Vitt KN, Kuzheleva EA, Tukish OV, et al. Low-intensity inflammation as a manifestation of comorbidity and a factor in the unfavorable clinical course of heart failure with preserved ejection fraction. Cardiovascular Therapy and Prevention. 2024;23(2):3847. doi: 10.15829/1728-8800-2024-3847
24. Ballak DB, Stienstra R, Tack CJ, et al. IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance. Cytokine. 2015;75(2):280–290. doi: 10.1016/j.cyto.2015.05.005
25. Reilly SM, Saltiel AR. Adapting to obesity with adipose tissue inflammation. Nat Rev Endocrinol. 2017;13(11):633–643. doi: 10.1038/nrendo.2017.90
26. Gao J, Xie Q, Wei T, et al. Nebivolol Improves Obesity-Induced Vascular Remodeling by Suppressing NLRP3 Activation. J Cardiovasc Pharmacol. 2019;73(5):326–333.
doi: 10.1097/FJC.0000000000000667
27. Belaya ZE, Belova KYu, Biryukova EV, et al. Federal clinical guidelines for diagnosis, treatment and prevention of osteoporosis. Osteoporosis and Bone Diseases. 2021;24(2):4–47. doi: 10.14341/osteo1293
28. Curtis E, Litwic A, Cooper C, et al. Determinants of Muscle and Bone Aging. J Cell Physiol. 2015;230(11):2618–2625. doi: 10.1002/jcp.25001
29. Lloyd BD, Williamson DA, Singh NA, et al. Recurrent and injurious falls in the year following hip fracture: a prospective study of incidence and risk factors from the Sarcopenia and Hip Fracture study. J Gerontol A Biol Sci Med Sci. 2009;64(5):599–609. doi: 10.1093/gerona/glp003
30. Pajarinen J, Lin T, Gibon E, et al. Mesenchymal stem cell-macrophage crosstalk and bone healing. Biomaterials. 2019;196:80–89. doi: 10.1016/j.biomaterials.2017.12.025
31. Raggatt LJ, Wullschleger ME, Alexander KA, et al. Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification. Am J Pathol. 2014;184(12):3192–3204. doi: 10.1016/j.ajpath.2014.08.017
32. Sebastián C, Herrero C, Serra M, et al. Telomere shortening and oxidative stress in aged macrophages results in impaired STAT5a phosphorylation. J Immunol.
2009;183(4):2356–2364. doi: 10.4049/jimmunol.0901131
33. Vi L, Baht GS, Soderblom EJ, et al. Macrophage cells secrete factors including LRP1 that orchestrate the rejuvenation of bone repair in mice. Nat Commun. 2018;9(1):5191.
doi: 10.1038/s41467-018-07666-0
34. Saul D, Khosla S. Fracture healing in the setting of endocrine diseases, aging, and cellular senescence. Endocr Rev. 2022;43(6):984–1002. doi: 10.1210/endrev/bnac008
35. Topolyanskaya SV. Interleukin 6 in aging and age-related diseases. Klinitsist. 2020;14(3–4):K633. doi: 10.17650/1818-8338-2020-14-3-4-К633
36. Ballesteros J, Rivas D, Duque G. The role of the kynurenine pathway in the pathophysiology of frailty, sarcopenia, and osteoporosis. Nutrients. 2023;15(14):3132.
doi: 10.3390/nu15143132
37. Ge Y, Huang M, Yao YM. Recent advances in the biology of IL-1 family cytokines and their potential roles in development of sepsis. Cytokine Growth F R. 2019;45:24–34.
doi: 10.1016/j.cytogfr.2018.12.004
38. Jiang N, An J, Yang K, et al. NLRP3 inflammasome: A new target for prevention and control of osteoporosis? Front Endocrinol (Lausanne). 2021;12:752546.
doi: 10.3389/fendo.2021.752546
39. Fischer J, Hans D, Lamy O, et al. "Inflammaging" and bone in the OsteoLaus cohort. Immun Ageing. 2020;17:5. doi: 10.1186/s12979-020-00177-x
40. Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell. 2015;14(4):644–658. doi: 10.1111/acel.12344
41. Morgunova GV, Khokhlov AN. Drugs with senolytic activity: prospects and possible limitations. Vestnik Moskovskogo universiteta. Seriya 16. Biologiya. 2023;78(4):278–284.
doi: 10.55959/MSU0137-0952-16-78-4-3
42. Toldo S, Mezzaroma E, Buckley LF, et al. Targeting the NLRP3 inflammasome in cardiovascular diseases. Pharmacol Ther. 2022; 236:108053. doi: 10.1016/j.pharmthera.2021.108053
43. Solomon SD, McMurray JJV, Anand IS, et al. Investigators and committees. angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609–1620. doi: 10.1056/NEJMoa1908655
44. Compston JE, McClung MR, Leslie WD. Osteoporosis. Lancet. 2019;393(10169):364–376. doi: 10.1016/S0140-6736(18)32112-3
2. Decade of healthy ageing: baseline report, 2021. В: World Health Organization [Internet]. Режим доступа: https://www.who.int/publicationsMem/9789240017900 Дата обращения: 23.02.2024.
3. Franceschi C., Bonafe M., Valensin S., et al. Inflamm-aging. An evolutionary perspective on immunosenescence // Ann N Y Acad Sci. 2000. Vol. 908. Р. 208–218.
doi: 10.1111/j.1749-6632.2000.tb06651.x
4. Savarese G., Becher P.M., Lund L.H., et al. Global burden of heart failure: a comprehensive and updated review of epidemiology // Cardiovasc Res. 2023. Vol. 118, N. 17.
Р. 3272–3287. doi: 10.1093/cvr/cvac013
5. Артемьева О.В., Ганковская Л.В. Воспалительное старение как основа возраст-ассоциированной патологии // Медицинская иммунология. 2020. Т. 22, № 3.
С. 419–432. doi: 10.15789/1563-0625-IAT-1938.
6. Артемьева О.В., Греченко В.В., Громова Т.В., и др. Синдром старческой астении: неоднозначная роль воспалительного старения // Иммунология. 2022. Т. 43, № 6.
С. 746–756. doi: 10.33029/0206-4952-2022-43-6-746-756
7. Montecino-Rodriguez E., Berent-Maoz B., Dorshkind K. Causes, consequences, and reversal of immune system aging // J Clin Invest. 2013. Vol. 123, N. 3. Р. 958–965.
doi: 10.1172/JCI64096
8. Bai L., Liu Y., Zhang X., et al. Osteoporosis remission via an anti-inflammaging effect by icariin activated autophagy // Biomaterials. 2023. Vol. 297. Р. 122–125.
doi: 10.1016/j.biomaterials.2023.122125
9. DeBerge M., Shah S.J., Wilsbacher L., et al. Macrophages in heart failure with reduced versus preserved ejection fraction // Trends Mol Med. 2019. Vol. 25, N. 4. Р. 328–340.
doi: 10.1016/j.molmed.2019.01.002
10. Mizushima N., Komatsu M. Autophagy: renovation of cells and tissues // Cell. 2011. Vol. 147, N. 4. Р. 728–741. doi: 10.1016/j.cell.2011.10.026
11. Chatterjee N., Walker G.C. Mechanisms of DNA damage, repair, and mutagenesis // Environ Mol Mutagen. 2017. Vol. 58, N. 5. Р. 235–263. doi: 10.1002/em.22087
12. Mezzaroma E., Toldo S., Farkas D., et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse // Proc Natl Acad Sci USA. 2011. Vol. 108, N. 49. Р. 19725–19730. doi: 10.1073/pnas.1108586108
13. Hulsmans M., Sager H.B., Roh J.D., et al. Cardiac macrophages promote diastolic dysfunction // J Exp Med. 2018. Vol. 215, N. 2. Р. 423–440. doi: 10.1084/jem.20171274
14. Liang Z., Zhang T., Liu H., et al. Inflammaging: The ground for sarcopenia? // Exp Gerontol. 2022. Vol. 68. Р. 111931. doi: 10.1016/j.exger.2022.111931
15. Antuña E., Cachán-Vega C., Bermejo-Millo J.C., et al. Inflammaging: Implications in Sarcopenia // Int J Mol Sci. 2022. Vol. 23, N. 23. Р. 15039. doi: 10.3390/ijms232315039
16. Ajoolabady A., Pratico D., Vinciguerra M., et al. Inflammaging: mechanisms and role in the cardiac and vasculature // Trends Endocrinol Metab. 2023. Vol. 34, N. 6. Р. 373–387.
doi: 10.1016/j.tem.2023.03.005
17. Казанова П.В., Басиева М.А., Шварц В.А. Иммунное ремоделирование в патогенезе фибрилляции предсердий // Анналы аритмологии. 2023. Т. 20, № 2. С. 119–130.
doi: 10.15275/annaritmol.2023.2.7
18. Yao Y., Yang M., Liu D., et al. Immune remodeling and atrial fibrillation // Front Physiol. 2022. Vol. 13. Р. 927221. doi: 10.3389/fphys.2022.927221
19. Ионин В.А., Барашкова Е.И., Заславская Е.Л., и др. Биомаркеры воспаления, параметры, характеризующие ожирение и ремоделирование сердца, у пациентов с фибрилляцией предсердий и метаболическим синдромом // Российский кардиологический журнал. 2021. Т. 26, № 3. С. 4343. doi: 10.15829/15604071-2021-4343
20. Santhanakrishnan R., Chong J.P., Ng T.P., et al. Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction // Eur J Heart Fail. 2012. Vol. 14, N. 12. Р. 1338–1347. doi: 10.1093/eurjhf/hfs130
21. Алиева А.М., Резник Е.В., Пинчук Т.В., и др. Фактор дифференцировки роста — 15 (GDF-15) как биологический маркер при сердечной недостаточности // Архивъ внутренней медицины. 2023. Т. 13, № 1. С. 14–23. doi: 10.20514/2226-6704-2023-13-1-14-23
22. Bouabdallaoui N., Claggett B., Zile M.R., et al. Growth differentiation factor-15 is not modified by sacubitril/valsartan and is an independent marker of risk in patients with heart failure and reduced ejection fraction: the PARADIGM-HF trial // Eur J Heart Fail. 2018. Vol. 20, N. 12. Р. 1701–1709. doi: 10.1002/ejhf.1301
23. Витт К.Н., Кужелева Е.А., Тукиш О.В., и др. Низкоинтенсивное воспаление как проявление коморбидности и фактор неблагоприятного клинического течения сердечной недостаточности с сохранённой фракцией выброса // Кардиоваскулярная терапия и профилактика. 2024. Т. 23, № 2. С. 3847. doi: 10.15829/1728-8800-2024-3847
24. Ballak D.B., Stienstra R., Tack C.J., et al. IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance // Cytokine. 2015. Vol. 75, N. 2. Р. 280–290. doi: 10.1016/j.cyto.2015.05.005
25. Reilly S.M., Saltiel A.R. Adapting to obesity with adipose tissue inflammation // Nat Rev Endocrinol. 2017. Vol. 13, N. 11. Р. 633–643. doi: 10.1038/nrendo.2017.90
26. Gao J., Xie Q., Wei T., et al. Nebivolol Improves Obesity-Induced Vascular Remodeling by Suppressing NLRP3 Activation // J Cardiovasc Pharmacol. 2019. Vol. 73, N. 5.
Р. 326–333. doi: 10.1097/FJC.0000000000000667
27. Белая Ж.Е., Белова К.Ю., Бирюкова Е.В., и др. Федеральные клинические рекомендации по диагностике, лечению и профилактике остеопороза // Остеопороз и остеопатии. 2021. Т. 24, № 2. С. 4–47. doi: 10.14341/osteo1293
28. Curtis E., Litwic A., Cooper C., et al. Determinants of Muscle and Bone Aging // J Cell Physiol. 2015. Vol. 230, N. 11. Р. 2618–2625. doi: 10.1002/jcp.25001
29. Lloyd B.D., Williamson D.A., Singh N.A., et al. Recurrent and injurious falls in the year following hip fracture: a prospective study of incidence and risk factors from the Sarcopenia and Hip Fracture study // J Gerontol A Biol Sci Med Sci. 2009. Vol. 64, N. 5. Р. 599–609. doi: 10.1093/gerona/glp003
30. Pajarinen J., Lin T., Gibon E., et al. Mesenchymal stem cell-macrophage crosstalk and bone healing // Biomaterials. 2019. Vol. 196. Р. 80–89. doi: 10.1016/j.biomaterials.2017.12.025
31. Raggatt L.J., Wullschleger M.E., Alexander K.A., et al. Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification // Am J Pathol. 2014. Vol. 184, N. 12. Р. 3192–3204. doi: 10.1016/j.ajpath.2014.08.017
32. Sebastián C., Herrero C., Serra M., et al. Telomere shortening and oxidative stress in aged macrophages results in impaired STAT5a phosphorylation // J Immunol. 2009. Vol. 183,
N. 4. Р. 2356–2364. doi: 10.4049/jimmunol.0901131
33. Vi L., Baht G.S., Soderblom E.J., et al. Macrophage cells secrete factors including LRP1 that orchestrate the rejuvenation of bone repair in mice // Nat Commun. 2018. Vol. 9, N. 1.
Р. 5191. doi: 10.1038/s41467-018-07666-0
34. Saul D., Khosla S. Fracture healing in the setting of endocrine diseases, aging, and cellular senescence // Endocr Rev. 2022. Vol. 43, N. 6. Р. 984–1002. doi: 10.1210/endrev/bnac008
35. Тополянская С.В. Роль интерлейкина 6 при старении и возрастассоциированных заболеваниях // Клиницист. 2020. Т. 14, № 3–4. С. К633.
doi: 10.17650/1818-8338-2020-14-3-4-К633
36. Ballesteros J., Rivas D., Duque G. The role of the kynurenine pathway in the pathophysiology of frailty, sarcopenia, and osteoporosis // Nutrients. 2023. Vol. 15, N. 14. Р. 3132.
doi: 10.3390/nu15143132
37. Ge Y., Huang M., Yao Y.M. Recent advances in the biology of IL-1 family cytokines and their potential roles in development of sepsis // Cytokine Growth F R. 2019. Vol. 45. Р. 24–34. doi: 10.1016/j.cytogfr.2018.12.004
38. Jiang N., An J., Yang K., et al. NLRP3 inflammasome: A new target for prevention and control of osteoporosis? // Front Endocrinol (Lausanne). 2021. Vol. 12. Р. 752546.
doi: 10.3389/fendo.2021.752546
39. Fischer J., Hans D., Lamy O., et al. "Inflammaging" and bone in the OsteoLaus cohort // Immun Ageing. 2020. Vol. 17. Р. 5. doi: 10.1186/s12979-020-00177-x
40. Zhu Y., Tchkonia T., Pirtskhalava T., et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs // Aging Cell. 2015. Vol. 14, N. 4. Р. 644–658.
doi: 10.1111/acel.12344
41. Моргунова Г.В., Хохлов А.Н. Препараты с сенолитической активностью: перспективы и возможные ограничения // Вестник Московского университета. Серия 16. Биология. 2023. Т. 78, № 4. С. 278–284. doi: 10.55959/MSU0137-0952-16-78-4-3
42. Toldo S., Mezzaroma E., Buckley L.F., et al. Targeting the NLRP3 inflammasome in cardiovascular diseases // Pharmacol Ther. 2022. Vol. 236. Р. 108053.
doi: 10.1016/j.pharmthera.2021.108053
43. Solomon S.D., McMurray J.J.V., Anand I.S., et al. Investigators and committees. angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction // N Engl J Med. 2019. Vol. 381, N. 17. Р. 1609–1620. doi: 10.1056/NEJMoa1908655
44. Compston J.E., McClung M.R., Leslie W.D. Osteoporosis // Lancet. 2019. Vol. 393, N. 10169. Р. 364–376. doi: 10.1016/S0140-6736(18)32112-3
________________________________________________
2. Decade of healthy ageing: baseline report, 2021. In: World Health Organization [Internet]. Available from: https://www.who.int/publicationsMem/9789240017900 Accessed: 23.02.2024.
3. Franceschi C, Bonafe M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:208–218.
doi: 10.1111/j.1749-6632.2000.tb06651.x
4. Savarese G, Becher PM, Lund LH, et al. Global burden of heart failure: a comprehensive and updated review of epidemiology. Cardiovasc Res. 2023;118(17):3272–3287.
doi: 10.1093/cvr/cvac013
5. Artemyeva OV, Gankovskaya LV, Inflammagingas the basis of age-associated diseases. Meditsinskaya Immunologiya. 2020;22(3):419–432. doi: 10.15789/1563-0625-IAT-1938
6. Artemyeva OV, Grechenko VV, Gromova TV, et al. Frailty: a controversial role of inflammaging. Immunologiya. 2022;43(6):746–56. doi: 10.33029/0206-4952-2022-43-6-746-756
7. Montecino-Rodriguez E, Berent-Maoz B, Dorshkind K. Causes, consequences, and reversal of immune system aging. J Clin Invest. 2013;123(3):958–965. doi: 10.1172/JCI64096
8. Bai L, Liu Y, Zhang X, et al. Osteoporosis remission via an anti-inflammaging effect by icariin activated autophagy. Biomaterials. 2023;297:122–125.
doi: 10.1016/j.biomaterials.2023.122125
9. DeBerge M, Shah SJ, Wilsbacher L, et al. Macrophages in heart failure with reduced versus preserved ejection fraction. Trends Mol Med. 2019;25(4):328–340.
doi: 10.1016/j.molmed.2019.01.002
10. Mizushima N, Komatsu M. Autophagy: renovation of cells and tissues. Cell. 2011;147(4):728–741. doi: 10.1016/j.cell.2011.10.026
11. Chatterjee N, Walker GC. Mechanisms of DNA damage, repair, and mutagenesis. Environ Mol Mutagen. 2017;58(5):235–263. doi: 10.1002/em.22087
12. Mezzaroma E, Toldo S, Farkas D, et al. The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse. Proc Natl Acad Sci USA. 2011;108(49):19725–19730. doi: 10.1073/pnas.1108586108
13. Hulsmans M, Sager HB, Roh JD, et al. Cardiac macrophages promote diastolic dysfunction. J Exp Med. 2018;215(2):423–440. doi: 10.1084/jem.20171274
14. Liang Z, Zhang T, Liu H, et al. Inflammaging: The ground for sarcopenia? Exp Gerontol. 2022;68:111931. doi: 10.1016/j.exger.2022.111931
15. Antuña E, Cachán-Vega C, Bermejo-Millo JC, et al. Inflammaging: Implications in Sarcopenia. Int J Mol Sci. 2022;23(23):15039. doi: 10.3390/ijms232315039
16. Ajoolabady A, Pratico D, Vinciguerra M, et al. Inflammaging: mechanisms and role in the cardiac and vasculature. Trends Endocrinol Metab. 2023;34(6):373–387.
doi: 10.1016/j.tem.2023.03.005
17. Kazanova PV, Basieva MA, Shvartz VA. Immune remodeling in the pathogenesis of atrial fibrillation. Annaly aritmologii. 2023;20(2):119–130. doi: 10.15275/annaritmol.2023.2.7
18. Yao Y, Yang M, Liu D, et al. Immune remodeling and atrial fibrillation. Front Physiol. 2022;13:927221. doi: 10.3389/fphys.2022.927221
19. Ionin VA, Barashkova EI, Zaslavskaya EL, et al. Biomarkers of inflammation, parameters characterizing obesity and cardiac remodeling in patients with atrial fibrillation and metabolic syndrome. Russian Journal of Cardiology. 2021;26(3):4343. doi: 10.15829/15604071-2021-4343
20. Santhanakrishnan R, Chong JP, Ng TP, et al. Growth differentiation factor 15, ST2, high-sensitivity troponin T, and N-terminal pro brain natriuretic peptide in heart failure with preserved vs. reduced ejection fraction. Eur J Heart Fail. 2012;14(12):1338–1347. doi: 10.1093/eurjhf/hfs130
21. Alieva AM, Reznik EV, Pinchuk TV, et al. Growth Differentiation Factor-15 (GDF-15) is a Biological Marker in Heart Failure. The Russian Archives of Internal Medicine.
2023;13(1):14–23. doi: 10.20514/2226-6704-2023-13-1-14-23
22. Bouabdallaoui N, Claggett B, Zile MR, et al. Growth differentiation factor-15 is not modified by sacubitril/valsartan and is an independent marker of risk in patients with heart failure and reduced ejection fraction: the PARADIGM-HF trial. Eur J Heart Fail. 2018;20(12):1701–1709. doi: 10.1002/ejhf.1301
23. Vitt KN, Kuzheleva EA, Tukish OV, et al. Low-intensity inflammation as a manifestation of comorbidity and a factor in the unfavorable clinical course of heart failure with preserved ejection fraction. Cardiovascular Therapy and Prevention. 2024;23(2):3847. doi: 10.15829/1728-8800-2024-3847
24. Ballak DB, Stienstra R, Tack CJ, et al. IL-1 family members in the pathogenesis and treatment of metabolic disease: Focus on adipose tissue inflammation and insulin resistance. Cytokine. 2015;75(2):280–290. doi: 10.1016/j.cyto.2015.05.005
25. Reilly SM, Saltiel AR. Adapting to obesity with adipose tissue inflammation. Nat Rev Endocrinol. 2017;13(11):633–643. doi: 10.1038/nrendo.2017.90
26. Gao J, Xie Q, Wei T, et al. Nebivolol Improves Obesity-Induced Vascular Remodeling by Suppressing NLRP3 Activation. J Cardiovasc Pharmacol. 2019;73(5):326–333.
doi: 10.1097/FJC.0000000000000667
27. Belaya ZE, Belova KYu, Biryukova EV, et al. Federal clinical guidelines for diagnosis, treatment and prevention of osteoporosis. Osteoporosis and Bone Diseases. 2021;24(2):4–47. doi: 10.14341/osteo1293
28. Curtis E, Litwic A, Cooper C, et al. Determinants of Muscle and Bone Aging. J Cell Physiol. 2015;230(11):2618–2625. doi: 10.1002/jcp.25001
29. Lloyd BD, Williamson DA, Singh NA, et al. Recurrent and injurious falls in the year following hip fracture: a prospective study of incidence and risk factors from the Sarcopenia and Hip Fracture study. J Gerontol A Biol Sci Med Sci. 2009;64(5):599–609. doi: 10.1093/gerona/glp003
30. Pajarinen J, Lin T, Gibon E, et al. Mesenchymal stem cell-macrophage crosstalk and bone healing. Biomaterials. 2019;196:80–89. doi: 10.1016/j.biomaterials.2017.12.025
31. Raggatt LJ, Wullschleger ME, Alexander KA, et al. Fracture healing via periosteal callus formation requires macrophages for both initiation and progression of early endochondral ossification. Am J Pathol. 2014;184(12):3192–3204. doi: 10.1016/j.ajpath.2014.08.017
32. Sebastián C, Herrero C, Serra M, et al. Telomere shortening and oxidative stress in aged macrophages results in impaired STAT5a phosphorylation. J Immunol.
2009;183(4):2356–2364. doi: 10.4049/jimmunol.0901131
33. Vi L, Baht GS, Soderblom EJ, et al. Macrophage cells secrete factors including LRP1 that orchestrate the rejuvenation of bone repair in mice. Nat Commun. 2018;9(1):5191.
doi: 10.1038/s41467-018-07666-0
34. Saul D, Khosla S. Fracture healing in the setting of endocrine diseases, aging, and cellular senescence. Endocr Rev. 2022;43(6):984–1002. doi: 10.1210/endrev/bnac008
35. Topolyanskaya SV. Interleukin 6 in aging and age-related diseases. Klinitsist. 2020;14(3–4):K633. doi: 10.17650/1818-8338-2020-14-3-4-К633
36. Ballesteros J, Rivas D, Duque G. The role of the kynurenine pathway in the pathophysiology of frailty, sarcopenia, and osteoporosis. Nutrients. 2023;15(14):3132.
doi: 10.3390/nu15143132
37. Ge Y, Huang M, Yao YM. Recent advances in the biology of IL-1 family cytokines and their potential roles in development of sepsis. Cytokine Growth F R. 2019;45:24–34.
doi: 10.1016/j.cytogfr.2018.12.004
38. Jiang N, An J, Yang K, et al. NLRP3 inflammasome: A new target for prevention and control of osteoporosis? Front Endocrinol (Lausanne). 2021;12:752546.
doi: 10.3389/fendo.2021.752546
39. Fischer J, Hans D, Lamy O, et al. "Inflammaging" and bone in the OsteoLaus cohort. Immun Ageing. 2020;17:5. doi: 10.1186/s12979-020-00177-x
40. Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell. 2015;14(4):644–658. doi: 10.1111/acel.12344
41. Morgunova GV, Khokhlov AN. Drugs with senolytic activity: prospects and possible limitations. Vestnik Moskovskogo universiteta. Seriya 16. Biologiya. 2023;78(4):278–284.
doi: 10.55959/MSU0137-0952-16-78-4-3
42. Toldo S, Mezzaroma E, Buckley LF, et al. Targeting the NLRP3 inflammasome in cardiovascular diseases. Pharmacol Ther. 2022; 236:108053. doi: 10.1016/j.pharmthera.2021.108053
43. Solomon SD, McMurray JJV, Anand IS, et al. Investigators and committees. angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609–1620. doi: 10.1056/NEJMoa1908655
44. Compston JE, McClung MR, Leslie WD. Osteoporosis. Lancet. 2019;393(10169):364–376. doi: 10.1016/S0140-6736(18)32112-3
Авторы
В.Н. Ларина, Е.С. Щербина*
Российский национальный исследовательский медицинский университет им. Н.И. Пирогова, Москва, Россия
*semushinamarina@yandex.ru
Pirogov Russian National Research Medical University, Moscow, Russia
*semushinamarina@yandex.ru
Российский национальный исследовательский медицинский университет им. Н.И. Пирогова, Москва, Россия
*semushinamarina@yandex.ru
________________________________________________
Pirogov Russian National Research Medical University, Moscow, Russia
*semushinamarina@yandex.ru
Цель портала OmniDoctor – предоставление профессиональной информации врачам, провизорам и фармацевтам.