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高迁移率族蛋白 B1 与自噬在糖尿病及其并发症发病机制中的关系。

The relationship between HMGB1 and autophagy in the pathogenesis of diabetes and its complications.

机构信息

College of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

College of Acupuncture and Massage, Beijing University of Chinese Medicine, Beijing, China.

出版信息

Front Endocrinol (Lausanne). 2023 Mar 29;14:1141516. doi: 10.3389/fendo.2023.1141516. eCollection 2023.

DOI:10.3389/fendo.2023.1141516
PMID:37065747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10090453/
Abstract

Diabetes mellitus is a chronic metabolic disorder characterized by elevated blood glucose levels and has become the third leading threat to human health after cancer and cardiovascular disease. Recent studies have shown that autophagy is closely associated with diabetes. Under normal physiological conditions, autophagy promotes cellular homeostasis, reduces damage to healthy tissues and has bidirectional effects on regulating diabetes. However, under pathological conditions, unregulated autophagy activation leads to cell death and may contribute to the progression of diabetes. Therefore, restoring normal autophagy may be a key strategy to treat diabetes. High-mobility group box 1 protein (HMGB1) is a chromatin protein that is mainly present in the nucleus and can be actively secreted or passively released from necrotic, apoptotic, and inflammatory cells. HMGB1 can induce autophagy by activating various pathways. Studies have shown that HMGB1 plays an important role in insulin resistance and diabetes. In this review, we will introduce the biological and structural characteristics of HMGB1 and summarize the existing knowledge on the relationship between HMGB1, autophagy, diabetes, and diabetic complications. We will also summarize potential therapeutic strategies that may be useful for the prevention and treatment of diabetes and its complications.

摘要

糖尿病是一种以高血糖为特征的慢性代谢性疾病,已成为继癌症和心血管疾病之后人类健康的第三大威胁。最近的研究表明,自噬与糖尿病密切相关。在正常生理条件下,自噬促进细胞内稳态,减少对健康组织的损伤,对调节糖尿病具有双向作用。然而,在病理条件下,不受调节的自噬激活可导致细胞死亡,并可能促进糖尿病的进展。因此,恢复正常的自噬可能是治疗糖尿病的关键策略。高迁移率族蛋白 B1(HMGB1)是一种染色质蛋白,主要存在于核内,可从坏死、凋亡和炎症细胞中主动分泌或被动释放。HMGB1 可通过激活多种途径诱导自噬。研究表明,HMGB1 在胰岛素抵抗和糖尿病中起重要作用。在本综述中,我们将介绍 HMGB1 的生物学和结构特征,并总结目前关于 HMGB1、自噬、糖尿病及其并发症之间关系的知识。我们还将总结可能对预防和治疗糖尿病及其并发症有用的潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/dcdf289342e8/fendo-14-1141516-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/d7862c197d21/fendo-14-1141516-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/dcdf289342e8/fendo-14-1141516-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/d7862c197d21/fendo-14-1141516-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/790d37620786/fendo-14-1141516-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/e3d7c70183e8/fendo-14-1141516-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/261b/10090453/dcdf289342e8/fendo-14-1141516-g004.jpg

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