Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке?
Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке?
Ахмедов В.А., Гаус О.В. Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке? Терапевтический архив. 2021; 93 (1): 66–70. DOI: 10.26442/00403660.2021.01.200595
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Akhmedov V.A., Gaus O.V. Inflammatory diseases of the pancreas: what new do we know about the mechanisms of their development in the 21st century? Terapevticheskii Arkhiv (Ter. Arkh.). 2021; 93 (1): 66–70. DOI: 10.26442/00403660.2021.01.200595
Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке?
Ахмедов В.А., Гаус О.В. Воспалительные заболевания поджелудочной железы: что нового мы знаем о механизмах их развития в XXI веке? Терапевтический архив. 2021; 93 (1): 66–70. DOI: 10.26442/00403660.2021.01.200595
________________________________________________
Akhmedov V.A., Gaus O.V. Inflammatory diseases of the pancreas: what new do we know about the mechanisms of their development in the 21st century? Terapevticheskii Arkhiv (Ter. Arkh.). 2021; 93 (1): 66–70. DOI: 10.26442/00403660.2021.01.200595
Воспалительные заболевания поджелудочной железы могут варьировать от острого до острого рецидивирующего и хронического панкреатита. С совершенствованием лабораторной диагностики в XXI в. стали более понятны механизмы провоспалительной и противовоспалительной роли плотных соединений, в частности трансмембранных белков окклюдина, клаудина и JAMs, цитоплазматических Zo-белков, а также адгезивных соединений, в частности α-катенина, β-катенина, Е-кадгерина, селектинов и ICAMs, в патогенезе острого и хронического панкреатита. Изучение генетических факторов развития острого и хронического панкреатита показало роль мутаций генов SPINK1 N34S, PRSS1, CEL-HYB в прогрессировании заболевания.
Inflammatory diseases of the pancreas can range from acute to acute recurrent and chronic pancreatitis. With the improvement of laboratory diagnostics in the 21st century, the mechanisms of the pro-inflammatory and anti-inflammatory role of tight junctions, in particular the transmembrane proteins occludin, claudine and JAMs, cytoplasmic Zo-proteins, and adherens junctions, in particular α-catenin, β-catenin, E-cadherin, selectins and ICAMs in the pathogenesis of acute and chronic pancreatitis have become more clear. The study of genetic factors in the development of acute and chronic pancreatitis showed the role of mutations in the genes SPINK1 N34S, PRSS1, CEL-HYB in the progression of the disease.
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________________________________________________
1. Machicado JD, Yadav D. Epidemiology of Recurrent Acute and Chronic Pancreatitis: Similarities and Differences. Dig Dis Sci. 2017;62(7):1683-91. doi: 10.1007/s10620-017-4510-5
2. Magnusdottir BA, Baldursdottir MB, Kalaitzakis E, Björnsson ES. Risk Factors for Chronic and Recurrent Pancreatitis After First Attack of Acute Pancreatitis. Scand J Gastroenterol. 2019;54(1):87-94. doi: 10.1080/00365521.2018.1550670
3. Stigliano S, Belisario F, Piciucchi M, et al. Recurrent Biliary Acute Pancreatitis Is Frequent in a Real-World Setting Dig Liver Dis. 2018;50(3):277-82. doi: 10.1016/j.dld.2017.12.011
4. El-Haija M, Valencia CA, Hornung L, et al. Genetic Variants in Acute, Acute Recurrent and Chronic Pancreatitis Affect the Progression of Disease in Children. Pancreatology. 2019;19(4):535-40. doi: 10.1016/j.pan.2019.05.001
5. Vinokurova LV, Shulyatev IS, Dubtsova EA, Agafonov MA. The importance of hereditary factors in the formation of complications in patients with chronic pancreatitis. Therapia. 2016;3(7):48-52 (In Russ.)
6. Maslovsky LV. Chronic pancreatitis New data. Med. sovet. 2016;14:32-5 (In Russ.)
doi: 10.21518/2079-701X-2016-14-32-35
7. Samgina TA, Kanishchev YuV, Al Isai Khanan SA, et al. The role of polymorphism (rs55754655) of the antioxidant system enzyme gene in the development of chronic pancreatitis. Kurskiy nauchno-prakticheskiy vestn. “Chelovek i yego zdorov'ye”. 2017;4:99-102 (In Russ.) doi: 10.21626/vestnik/2017-4/17
8. Samgina TA, Kanishchev YV, Grigor’yev SN, et al. The role of polymorphism (rs1800566) of NAD(F)H quinone oxidoreductase-1 in the development of acute pancreatitis. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2018;28(1):20-5 (In Russ.) doi: 10.22416/1382-4376-2018-28-1-20-25
9. Samgina TA, Zhivotova GA, Nazarenko PM, Polonikov AV. The role of cytokine genetic polymorphism in development of acute pancreatitis: analysis of intergenic and environmental interactions. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2017;27(3):27-33 (In Russ.) doi: 10.22416/1382-4376-2017-27-3-27-33
10. Samgina TA, Azarova YuE, Kanishchev YuV, et al. The Role of Phosphatidylethanolamine-N-methyltransferase (PEMT) Gene rs12449964 Polymorphism in the Development of Acute Pancreatitis and its Complications. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2019;29(5):21-5 (In Russ.) doi: 10.22416/1382-4376-2019-29-5-21-25
11. Menshikova EA, SHtaborov VA. Immune responses in exacerbation of chronic pancreatitis and gastric ulcer. Ros. immunologicheskiy zhurn. 2016;10(19):187-9 (In Russ.)
12. Sankaran SJ, Xiao AY, Wu LM, et al. Frequency of Progression From Acute to Chronic Pancreatitis and Risk Factors: A Meta-Analysis. Gastroenterology. 2015;149(6):1490-500. doi: 10.1053/j.gastro.2015.07.066
13. Hartsock A, Nelson WJ. Adherens and Tight Junctions: Structure, Function and Connections to the Actin Cytoskeleton. Biochim Biophys Acta. 2008;1778(3):660-9. doi: 10.1016/j.bbamem.2007.07.012
14. Zhang Z, Wang Y, Dong M, et al. Oxymatrine Ameliorates L-arginine-induced Acute Pancreatitis in Rats. Inflammation. 2012;35(2):605-13. doi: 10.1007/s10753-011-9352-2
15. Barbeiro DF, Koike MK, Coelh AM, et al. Intestinal Barrier Dysfunction and Increased COX-2 Gene Expression in the Gut of Elderly Rats With Acute Pancreatitis. Pancreatology. 2016;16(1):52-6. doi: 10.1016/j.pan.2015.10.012
16. Schmitt M, Klonowski-Stumpe H, Eckert M, et al. Disruption of Paracellular Sealing Is an Early Event in Acute Caerulein-Pancreatitis. Pancreas. 2004;28(2):181-90. doi: 10.1097/00006676-200403000-00010
17. Xia XM, Li BK, Xing SM, Ruan HL. Emodin Promoted Pancreatic claudin-5 and Occludin Expression in Experimental Acute Pancreatitis Rats. World J Gastroenterol. 2012;18(17):2132-9. doi: 10.3748/wjg.v18.i17.2132
18. Fallon MB, Gorelick FS, Anderson JM, et al. Effect of Cerulein Hyperstimulation on the Paracellular Barrier of Rat Exocrine Pancreas. Gastroenterology. 1995;108(6):1863-72. doi: 10.1016/0016-5085(95)90151-5
19. Wei Q, Huang H. Insights Into the Role of Cell-Cell Junctions in Physiology and Disease. Int Rev Cell Mol Biol. 2013;306:187-221. doi: 10.1016/B978-0-12-407694-5.00005-5
20. Vonlaufen A, Aurrand-Lions M, Pastor CM, et al. The Role of Junctional Adhesion Molecule C (JAM-C) in Acute Pancreatitis. J Pathol. 2006;209(4):540-8. doi: 10.1002/path.2007
21. Wu D, Zeng Y, Fan Y, et al. Reverse-migrated Neutrophils Regulated by JAM-C Are Involved in Acute Pancreatitis-Associated Lung Injury. Sci Rep. 2016;6:20545. doi: 10.1038/srep20545
22. Kojima T, Yamaguchi H, Ito T, et al. Tight Junctions in Human Pancreatic Duct Epithelial Cells. Tissue Barriers. 2013;1(4):e24894. doi: 10.4161/tisb.24894
23. Nakada S, Tsuneyama K, Kato I, et al. Identification of Candidate Genes Involved in Endogenous Protection Mechanisms Against Acute Pancreatitis in Mice. Biochem Biophys Res Commun. 2010;391(3):1342-7. doi: 10.1016/j.bbrc.2009.12.047
24. Xia XM, Li BK, Xing SM, Ruan HL. Emodin Promoted Pancreatic claudin-5 and Occludin Expression in Experimental Acute Pancreatitis Rats. World J Gastroenterol. 2012;18(17):2132-9. doi: 10.3748/wjg.v18.i17.2132
25. Gloushankova NA, Rubtsova SN, Zhitnyak IY. Cadherin-mediated Cell-Cell Interactions in Normal and Cancer Cells. Tissue Barriers. 2017;5(3):e1356900. doi: 10.1080/21688370.2017.1356900
26. Schnekenburger J, Mayerle J, Krüger B, et al. Protein Tyrosine Phosphatase Kappa and SHP-1 Are Involved in the Regulation of Cell-Cell Contacts at Adherens Junctions in the Exocrine Pancreas. Gut. 2005;54(10):1445-55. doi: 10.1136/gut.2004.063164
27. Cleveland MH, Sawyer JM, Afelik S, et al. Exocrine Ontogenies: On the Development of Pancreatic Acinar, Ductal and Centroacinar Cells. Semin Cell Dev Biol. 2012;23(6):711-9. doi: 10.1016/j.semcdb.2012.06.008
28. Heiser PW, Lau J, Taketo MM, et al Stabilization of Beta-Catenin Impacts Pancreas Growth. Development. 2006;133(10):2023-32. doi: 10.1242/dev.023662
29. Yuan W, Pan QI , Chen G, et al. E-cadherin Expression in a Rat Model of Acute Pancreatitis. Exp Ther Med. 2015;10(6):2088-92. doi: 10.3892/etm.2015.2786
30. Leckband DE, de Rooij J. Cadherin Adhesion and Mechanotransduction. Annu Rev Cell Dev Biol. 2014;30:291-315. doi: 10.1146/annurev-cellbio-100913-013212
31. Leser J, Beil MF, Musa OA, et al. Regulation of Adherens Junction Protein p120(ctn) by 10 nM CCK Precedes Actin Breakdown in Rat Pancreatic Acini. Am J Physiol Gastrointest Liver Physiol. 2000;278(3):486-91. doi: 10.1152/ajpgi.2000.278.3.G486
32. Hendley AM, Provost E, Bailey JM, et al. p120 Catenin Is Required for Normal Tubulogenesis but Not Epithelial Integrity in Developing Mouse Pancreas. Dev Biol. 2015;399(1):41-53. doi: 10.1016/j.ydbio.2014.12.010
33. Staubli SM, Oertli D, Nebiker CA. Laboratory Markers Predicting Severity of Acute Pancreatitis. Crit Rev Clin Lab Sci. 2015;52(6):273-83. doi: 10.3109/10408363.2015.1051659
34. Siemiatkowski A, Wereszczynska-Siemiatkowska U, Mroczko B, et al. Circulating Endothelial Mediators in Human Pancreatitis-Associated Lung Injury. Eur J Gastroenterol Hepatol. 2015;27(6):728-34. doi: 10.1097/MEG.0000000000000338
35. Hackert T, Sperber R, Hartwig W, et al. P-selectin Inhibition Reduces Severity of Acute Experimental Pancreatitis. Pancreatology. 2009;9(4):369-74. doi: 10.1159/000212098
36. Chen Y, Ke L, Meng L, et al. Endothelial Markers Are Associated With Pancreatic Necrosis and Overall Prognosis in Acute Pancreatitis: A Preliminary Cohort Study. Pancreatology. 2017;17(1):45-50. doi: 10.1016/j.pan.2016.12.005
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Авторы
В.А. Ахмедов, О.В. Гаус
ФГБОУ ВО «Омский государственный медицинский университет» Минздрава России, Омск, Россия