gastro-jРоссийский журнал гастроэнтерологии, гепатологии, колопроктологииRussian Journal of Gastroenterology, Hepatology, Coloproctology1382-43762658-6673«Gastro» LLC10.22416/1382-4376-2016-26-2-6-10gastro-j-28Research ArticleЛЕКЦИИ И ОБЗОРЫLECTURES AND REVIEWSРоль дисфункции митохондрий и лизосом в патогенезе острого панкреатитаRole of mitochondrial and lysosomal dysfunction in acute pancreatitis pathogenesisЕвсютинаЮлия ВикторовнаYevsyutinaYuliya Vuselina@mail.ruИвашкинВладимир ТрофимовичIvashkinV. T.noemail@neicon.ruАбгаджаваЭ. З.AbgadzhavaE. Z.noemail@neicon.ruГБОУ ВПО «Первый Московский государственный медицинский университет им. И.М. Сеченова»РоссияState educational government-financed institution of higher professional education «Sechenov First Moscow state medical university»Russian FederationРеспубликанская больница г. СухумРоссияSukhumi Republic hospitalRussian Federation201612082016262610Copyright © Евсютина Ю.В., Ивашкин В.Т., Абгаджава Э.З., 20162016Евсютина Ю.В., Ивашкин В.Т., Абгаджава Э.З.Yevsyutina Y.V., Ivashkin V.T., Abgadzhava E.Z.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.gastro-j.ru/jour/article/view/28

Цель обзора. Представить данные о роли дисфункции митохондрий и лизосом в патогенезе острого панкреатита (ОП). Основные положения. Основными патоморфологическими признаками ОП являются: гиперамилаземия, преждевременная интраацинарная активация пищеварительных ферментов, накопление крупных вакуолей в ацинарных клетках, активация провоспалительных медиаторов, гибель ацинарных клеток путем апоптоза и некроза. Дисфункция митохондрий, развивающаяся при остром панкреатите, сопровождается нарушением синтеза АТФ и инициацией процессов апоптоза и некроза. Дисфункция лизосом при ОП проявляется нарушением аутофагии, что приводит к вакуолизации ацинарных клеток иинтраацинарному накоплению трипсина. Заключение. В последнее время отмечаются рост заболеваемости острым панкреатитом и повышение смертности у пациентов с панкреонекрозом. Нарушение функции митохондрий и лизосом составляет патогенетическую основу ОП, приводя кдеэнергизации клеток поджелудочной железы. Дисфункция митохондрий и лизосом инициирует при рассматриваемой патологии процессы апоптоза, некроза, активацию трипсиногена и вакуолизацию ацинарных клеток. Необходимо проведение новых исследований, целью которых будет разработка стратегий терапевтического воздействия на митохондрии и лизосомы. Ключевые слова: острый панкреатит, дисфункция органелл, митохондрия, лизосома, апоптоз, некроз, аутофагия.

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.

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The authors declare that there are no conflicts of interest present.