diaendoСахарный диабетDiabetes mellitus2072-03512072-0378Endocrinology research centre10.14341/DM10242diaendo-10242Research ArticleОбзорыReviewСигнальные пути гибели β-клеток при сахарном диабете 2 типа: роль врожденного иммунитетаSignaling pathways of β-cell death in type 2 diabetes mellitus: the role of innate immunityhttps://orcid.org/0000-0002-2612-5253КалмыковаЗиля АсхатовнаKalmykovаZilya. A.

аспирант

MD, PhD student

zilya.kalmykova@gmail.comhttps://orcid.org/0000-0003-4929-1526КононенкоИрина ВладимировнаKononenkoIrina V.

к.м.н., в.н.с.

MD, PhD, leading research associate

shakhtarina@bk.ruhttps://orcid.org/0000-0003-3885-8988СмирноваОльга МихайловнаSmirnovaOlga M.

д.м.н., профессор, гл.н.с.

MD, PhD, Professor, chief research associate

dr_smr@mail.ruhttps://orcid.org/0000-0002-5057-127XШестаковаМарина ВладимировнаShestakovaMarina Vladimirovna

д.м.н., профессор, академик РАН

MD, PhD, Professor

nephro@endocrincentr.ruНациональный медицинский исследовательский центр эндокринологииРоссияEndocrinology Research CentreRussian Federation202026062020232174184Copyright © Калмыкова З.А., Кононенко И.В., Смирнова О.М., Шестакова М.В., 20202020Калмыкова З.А., Кононенко И.В., Смирнова О.М., Шестакова М.В.Kalmykovа Z.A., Kononenko I.V., Smirnova O.M., Shestakova M.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.dia-endojournals.ru/jour/article/view/10242

Сахарный диабет 2 типа (СД2) – мультифакторное обменное заболевание, развитие которого опосредовано как генетическими нарушениями, так и различными внутри- и внеклеточными молекулярными процессами. Одним из основных патогенетических механизмов развития СД2 является прогрессирующее снижение массы и функционального резерва β-клеток, которое во многом определяет течение СД2. Действие большинства сахароснижающих препаратов заключается в усилении секреции инсулина, поэтому очевидно, что эффективность проводимой терапии также во многом будет зависеть от функционального состояния β-клеток. Все это объясняет большой интерес к изучению механизмов повреждения и гибели β-клеток при СД2, а также факторов, которые могут ускорять данный процесс, приводя к развитию сначала относительного, а затем и абсолютного дефицита инсулина.

Механизмы, ведущие к ухудшению функционального состояния β-клеток при СД2, на сегодняшний день практически не изучены. В данной статье приведен обзор отечественной и зарубежной литературы последних лет о молекулярных, внутриклеточных особенностях различных механизмов повреждения и гибели β-клеток при СД2. Представлены результаты исследований, направленных на изучение возможных факторов и процессов, ведущих к их запуску.

Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disease, the development of which is mediated by both genetic disorders and various intracellular and extracellular molecular processes. One of the main pathogenetic mechanisms for the development of T2DM is a progressive decrease in the mass and functional reserve of β-cells, which largely determines the course of T2DM. The mechanisms of action of most sugar-lowering drugs are associated with increased secretion of insulin, so it is obvious that the effectiveness of the therapy will also largely depend on the functional state of β-cells. All this explains the great interest in studying the mechanisms of damage of β-cells in T2DM and factors that can accelerate this process, leading to their death and the development of a relative and then absolute insulin deficiency. The mechanisms of dysfunction β-cells in T2DM have not been studied much. This article provides an overview of the data of domestic and foreign literature of recent years on the molecular, intracellular features of various mechanisms of damage and death of β-cells in type 2 diabetes. The results of studies aimed at studying the possible factors and processes leading to their launch are presented.

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