Genes & CellsGenes & CellsГены и КлеткиGenes and Cells2313-18292500-2562Human Stem Cells Institute12072010.23868/201808017ArticlesСтатьиResearch ArticleProgrammed necrosis and tissue regenerationПрограммируемый некроз и регенерация тканейKopeinaG. SКопеинаГ. СZamaraevA. VЗамараевА. ВZhivotovskyB. DЖивотовскийБ. ДLavrikI. NЛаврикИ. НM.V. Lomonosov Moscow State UniversityМосковский государственный университет им. М.В. ЛомоносоваInstitute of Environmental Medicine, Karolinska InstituteИнститут медицины окружающей среды, Каролинский институт15062018132VOL 13, NO2 (2018)ТОМ 13, №2 (2018)353805012023Copyright ©; 2018, Eco-VectorCopyright ©; 2018, Эко-Вектор2018Eco-VectorЭко-Векторhttps://genescells.ru/2313-1829/article/view/120720

Programmed necrosis or necroptosis plays an important role in cell physiology. Disturbances in necroptotic process are associated with excessive cell death, the development of a number of pathological conditions, including inflammatory and neurodegenerative diseases. Accumulated evidences suggest the involvement of necroptosis in the induction of stem cell proliferation and tissue regeneration. The necrotic death can be triggered through the family of receptors of tumor necrosis factor, TRAILR1/2, FAS, as well as endosomal Toll-like and NOD-like receptors. An important role in the regulation of necroptosis belongs to proteins RIPK1 and RIPK3, which also might be essential for proliferation of stem cells and the regeneration process. Recent study has shown that necroptosis can lead to rapid activation of progenitor cells and regeneration of the hepatic tissues, as well as a necrotic-induced tissue regeneration and differentiation of c-kit+ cells in a model of myocardial infarction. Thus, the investigation of interplay between necroptosis and regeneration of damaged tissues will allow us to understand the fundamental aspects of programmed cell death and cell division.

Програмируемый некроз или некроптоз, играет существенную роль в физиологических процессах в организме. Нарушение процесса некроптоза связано с избыточной гибелью клеток, развитием ряда патологических состояний, включая воспалительные и нейродегенеративные заболевания. В последнее время появляются данные об участии некроптоза в индукции пролиферации стволовых клеток и регенерации тканей. Запуск некроптотической гибели может осуществляться через рецепторы фактора некроза опухоли, TRAILR1/2, FAS, а также через эндосомальные Toll-подобные и NOD-подобные рецепторы. Основные механизмы регуляции некроптотической гибели осуществляются на уровне главных белков - RIPK1 и RIPK3, которые способны принимать участие в пролиферации стволовых клеток и процессе регенерации. Последние работы показали, что некротические процессы могут приводить к быстрой активации клеток-предшественниц и регенерации печени, а также на модели инфаркта миокарда была продемонстрирована некроптоз-индуцированная регенерация ткани и дифференцировка c-kit+ клеток. Таким образом, изучение механизмов взаимосвязи некроптоза и регенерации поврежденных тканей позволит лучше понять фундаментальные аспекты программируемой гибели и деления клеток.

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