Effective protective mechanisms of HO-1 in diabetic complications: a narrative review.

IF 6.1 2区 生物学 Q1 CELL BIOLOGY
Jing-Jing Zhang, Ping Ni, Yi Song, Man-Jun Gao, Xi-Ying Guo, Bao-Qing Zhao
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引用次数: 0

Abstract

Diabetes mellitus is a metabolic disorder with persistent hyperglycemia caused by a variety of underlying factors. Chronic hyperglycemia can lead to diverse serious consequences and diversified complications, which pose a serious threat to patients. Among the major complications are cardiovascular disease, kidney disease, diabetic foot ulcers, diabetic retinopathy, and neurological disorders. Heme oxygenase 1 (HO-1) is a protective enzyme with antioxidant, anti-inflammatory and anti-apoptotic effects, which has been intensively studied and plays an important role in diabetic complications. By inducing the expression and activity of HO-1, it can enhance the antioxidant, anti-inflammatory, and anti-apoptotic capacity of tissues, and thus reduce the degree of damage in diabetic complications. The present study aims to review the relationship between HO-1 and the pathogenesis of diabetes and its complications. HO-1 is involved in the regulation of macrophage polarization and promotes the M1 state (pro-inflammatory) towards to the M2 state (anti-inflammatory). Induction of HO-1 expression in dendritic cells inhibits them maturation and secretion of pro-inflammatory cytokines and promotes regulatory T cell (Treg cell) responses. The induction of HO-1 can reduce the production of reactive oxygen species, thereby reducing oxidative stress and inflammation. Besides, HO-1 also has an important effect in novel programmed cell death such as pyroptosis and ferroptosis, thereby playing a protective role against diabetes. In conclusion, HO-1 plays a significant role in the occurrence and development of diabetic complications and is closely associated with a variety of complications. HO-1 is anticipated to serve as a novel target for addressing diabetic complications, and it holds promise as a potential therapeutic agent for diabetes and its associated complications. We hope to provide inspiration and ideas for future studies in the mechanism and targets of HO-1 through this review.

HO-1 在糖尿病并发症中的有效保护机制:综述。
糖尿病是由多种潜在因素引起的持续性高血糖代谢紊乱。长期高血糖可导致多种严重后果和多种并发症,对患者构成严重威胁。主要并发症包括心血管疾病、肾脏疾病、糖尿病足溃疡、糖尿病视网膜病变和神经系统疾病。血红素加氧酶 1(HO-1)是一种具有抗氧化、抗炎和抗细胞凋亡作用的保护性酶,已被深入研究,并在糖尿病并发症中发挥着重要作用。通过诱导 HO-1 的表达和活性,可以增强组织的抗氧化、抗炎和抗凋亡能力,从而减轻糖尿病并发症的损伤程度。本研究旨在回顾 HO-1 与糖尿病及其并发症发病机制的关系。HO-1参与调节巨噬细胞的极化,并促进M1状态(促炎)向M2状态(抗炎)转变。诱导树突状细胞表达 HO-1 可抑制树突状细胞的成熟和促炎细胞因子的分泌,并促进调节性 T 细胞(Treg 细胞)的反应。诱导 HO-1 可以减少活性氧的产生,从而减轻氧化应激和炎症反应。此外,HO-1 在新型程序性细胞死亡(如热凋亡和铁凋亡)中也有重要作用,从而对糖尿病起到保护作用。总之,HO-1 在糖尿病并发症的发生和发展中起着重要作用,并与多种并发症密切相关。HO-1有望成为解决糖尿病并发症的新靶点,并有望成为糖尿病及其相关并发症的潜在治疗药物。我们希望通过这篇综述为今后研究 HO-1 的机制和靶点提供灵感和思路。
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来源期刊
Cell Death Discovery
Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
8.30
自引率
1.40%
发文量
468
审稿时长
9 weeks
期刊介绍: Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
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