Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis
Aim of review. To present data on the role of mitochondrial and lysosomal dysfunction in pathogenesis of acute pancreatitis (AP). Summary. Hyperamilasemia, premature intralobular activation of digestive enzymes, accumulation of large vacuoles in acinar cells, activation of proinflammatory mediators,...
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Gastro LLC
2016-08-01
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Series: | Российский журнал гастроэнтерологии, гепатологии, колопроктологии |
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Online Access: | https://www.gastro-j.ru/jour/article/view/28 |
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author | Yuliya V Yevsyutina V. T. Ivashkin E. Z. Abgadzhava |
author_facet | Yuliya V Yevsyutina V. T. Ivashkin E. Z. Abgadzhava |
author_sort | Yuliya V Yevsyutina |
collection | DOAJ |
description | Aim of review. To present data on the role of mitochondrial and lysosomal dysfunction in pathogenesis of acute pancreatitis (AP). Summary. Hyperamilasemia, premature intralobular activation of digestive enzymes, accumulation of large vacuoles in acinar cells, activation of proinflammatory mediators, apoptosis and necrosis of acinar cells are the basic pathomorphological signs of AP. The mitochondrial dysfunction that develops at acute pancreatitis is followed by disorders of ATP synthesis and initiation of processes of apoptosis and necrosis. The lysosomal dysfunction at AP is manifested by autophagy disorders that leads to vacuolation of acinar cells and intralobular trypsin accumulation. Conclusion. At the recent time there is noticeable growth in frequency of acute pancreatitis cases and increase of mortality in patients with pancreatic necrosis. Mitochondrial and lysosomal dysfunction acts as pathogenic basis for AP, leading to energy deprivation of pancreatic cells. Mitochondrial and lysosomal dysfunction initiates processes of apoptosis, necrosis, activation of trypsinogen and vacuolation of acinar cells that this disease. Therefore new studies aimed for therapeutic impact on mitochondrions and lysosomes are required. Key words: acute pancreatitis, dysfunction of organellas, mitochondrion, lysosome, apoptosis, necrosis, autophagy. |
format | Article |
id | doaj-art-a6ccd2b86c524bca8b9398cb2a19b8d0 |
institution | Kabale University |
issn | 1382-4376 2658-6673 |
language | Russian |
publishDate | 2016-08-01 |
publisher | Gastro LLC |
record_format | Article |
series | Российский журнал гастроэнтерологии, гепатологии, колопроктологии |
spelling | doaj-art-a6ccd2b86c524bca8b9398cb2a19b8d02025-02-10T16:14:34ZrusGastro LLCРоссийский журнал гастроэнтерологии, гепатологии, колопроктологии1382-43762658-66732016-08-0126261010.22416/1382-4376-2016-26-2-6-1028Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesisYuliya V Yevsyutina0V. T. Ivashkin1E. Z. Abgadzhava2State educational government-financed institution of higher professional education «Sechenov First Moscow state medical university»State educational government-financed institution of higher professional education «Sechenov First Moscow state medical university»Sukhumi Republic hospitalAim of review. To present data on the role of mitochondrial and lysosomal dysfunction in pathogenesis of acute pancreatitis (AP). Summary. Hyperamilasemia, premature intralobular activation of digestive enzymes, accumulation of large vacuoles in acinar cells, activation of proinflammatory mediators, apoptosis and necrosis of acinar cells are the basic pathomorphological signs of AP. The mitochondrial dysfunction that develops at acute pancreatitis is followed by disorders of ATP synthesis and initiation of processes of apoptosis and necrosis. The lysosomal dysfunction at AP is manifested by autophagy disorders that leads to vacuolation of acinar cells and intralobular trypsin accumulation. Conclusion. At the recent time there is noticeable growth in frequency of acute pancreatitis cases and increase of mortality in patients with pancreatic necrosis. Mitochondrial and lysosomal dysfunction acts as pathogenic basis for AP, leading to energy deprivation of pancreatic cells. Mitochondrial and lysosomal dysfunction initiates processes of apoptosis, necrosis, activation of trypsinogen and vacuolation of acinar cells that this disease. Therefore new studies aimed for therapeutic impact on mitochondrions and lysosomes are required. Key words: acute pancreatitis, dysfunction of organellas, mitochondrion, lysosome, apoptosis, necrosis, autophagy.https://www.gastro-j.ru/jour/article/view/28острый панкреатитдисфункция органеллмитохондриялизосомаапоптознекрозаутофагия |
spellingShingle | Yuliya V Yevsyutina V. T. Ivashkin E. Z. Abgadzhava Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis Российский журнал гастроэнтерологии, гепатологии, колопроктологии острый панкреатит дисфункция органелл митохондрия лизосома апоптоз некроз аутофагия |
title | Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
title_full | Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
title_fullStr | Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
title_full_unstemmed | Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
title_short | Role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
title_sort | role of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesis |
topic | острый панкреатит дисфункция органелл митохондрия лизосома апоптоз некроз аутофагия |
url | https://www.gastro-j.ru/jour/article/view/28 |
work_keys_str_mv | AT yuliyavyevsyutina roleofmitochondrialandlysosomaldysfunctioninacutepancreatitispathogenesis AT vtivashkin roleofmitochondrialandlysosomaldysfunctioninacutepancreatitispathogenesis AT ezabgadzhava roleofmitochondrialandlysosomaldysfunctioninacutepancreatitispathogenesis |