Alanazi Yousef Abud, Al-Kuraishy Haydar M, Al-Gareeb Ali I, Alexiou Athanasios, Papadakis Marios, Bahaa Mostafa M, Negm Walaa A, AlAnazi Faisal Holil, Alrouji Mohammed, Batiha Gaber El-Saber
Department of Pediatrics, College of Medicine, Majmaah University, Majmaah, Saudi Arabia.
Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
J Cell Mol Med. 2024 Dec;28(23):e70240. doi: 10.1111/jcmm.70240.
Type 2 diabetes mellitus (T2DM) is developed due to the development of insulin resistance (IR) and pancreatic β cell dysfunction with subsequent hyperglycaemia. Hyperglycaemia-induced oxidative stress and endoplasmic reticulum (ER) stress enhances inflammatory disorders, leading to further pancreatic β cell dysfunction. These changes trigger autophagy activation, which recycles cytoplasmic components and injured organelles. Autophagy regulates pancreatic β cell functions by different mechanisms. Though the exact role of autophagy in T2DM is not completely elucidated, that could be beneficial or detrimental. Therefore, this review aims to discuss the exact role of autophagy in the pathogenesis of T2DM.
2型糖尿病(T2DM)是由于胰岛素抵抗(IR)和胰腺β细胞功能障碍的发展以及随后的高血糖症而发生的。高血糖诱导的氧化应激和内质网(ER)应激会加剧炎症紊乱,导致胰腺β细胞功能进一步受损。这些变化触发自噬激活,自噬可循环利用细胞质成分和受损细胞器。自噬通过不同机制调节胰腺β细胞功能。尽管自噬在T2DM中的确切作用尚未完全阐明,但它可能是有益的或有害的。因此,本综述旨在探讨自噬在T2DM发病机制中的确切作用。