Beta-cell autophagy under the scope of hypoglycemic drugs; possible mechanism as a novel therapeutic target
| Autor: | B. A. Marzoog, T. I. Vlasova |
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| Jazyk: | English<br />Russian |
| Rok vydání: | 2022 |
| Předmět: | |
| Zdroj: | Ожирение и метаболизм, Vol 18, Iss 4, Pp 465-470 (2022) |
| Druh dokumentu: | article |
| ISSN: | 2071-8713 2306-5524 |
| DOI: | 10.14341/omet12778 |
| Popis: | Physiologically, autophagy is a major protective mechanism of β-cells from apoptosis, through can reserve normal β- cell mass and inhibit the progression of β-cells destruction. Beta-cell mass can be affected by differentiation from progenitors and de-differentiation as well as self-renewal and apoptosis. Shred evidence indicated that hypoglycemic drugs can induce β-cell proliferation capacity and neogenesis via autophagy stimulation. However, prolonged use of selective hypoglycemic drugs has induced pancreatitis besides several other factors that contribute to β-cell destruction and apoptosis initiation. Interestingly, some nonhypoglycemic medications possess the same effects on β-cells but depending on the combination of these drugs and the duration of exposure to β-cells. The paper comprehensively illustrates the role of the hypoglycemic drugs on the insulin-producing cells and the pathogeneses of β-cell destruction in type 2 diabetes mellitus, in addition to the regulation mechanisms of β-cells division in norm and pathology. The grasping of the hypoglycemic drug’s role in beta-cell is clinically crucial to evaluate novel therapeutic targets such as new signaling pathways. The present paper addresses a new strategy for diabetes mellitus management via targeting specific autophagy inducer factors (transcription factors, genes, lipid molecules, etc.). |
| Databáze: | Directory of Open Access Journals |
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