糖尿病神经病变中的线粒体功能障碍：丝裂噬功能受损引发 NLRP3 炎性体。

IF 3.9 3区生物学 Q2 CELL BIOLOGY

Mitochondrion Pub Date : 2024-10-02 DOI:10.1016/j.mito.2024.101972

Keshari Sriwastawa, Ashutosh Kumar

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引用次数: 0

摘要

糖尿病神经病变是具有挑战性的糖尿病并发症之一，其特征是糖尿病高血糖导致的周围神经损伤。据报道，线粒体功能障碍是导致糖尿病神经病变中神经损伤的关键病理生理因素，临床表现为神经退行性病变以及功能和感觉运动障碍。越来越多的证据表明，线粒体功能障碍与 NLRP3 炎症小体激活之间存在明显的相关性。揭示线粒体功能障碍更深层次的分子方面可能会提供稳定有效的替代治疗方法。本综述将线粒体功能障碍联系起来，并评估其在糖尿病神经病变的病理生理学中的作用。我们还试图阐明线粒体吞噬在实验性糖尿病神经病变中激活 NLRP3 炎性体的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Mitochondrial dysfunction in diabetic neuropathy: Impaired mitophagy triggers NLRP3 inflammasome

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Mitochondrial dysfunction in diabetic neuropathy: Impaired mitophagy triggers NLRP3 inflammasome

Diabetic neuropathy is one of the challenging complications of diabetes and is characterized by peripheral nerve damage due to hyperglycemia in diabetes. Mitochondrial dysfunction has been reported as one of the key pathophysiological factor contributing to nerve damage in diabetic neuropathy, clinically manifesting as neurodegenerative changes like functional and sensorimotor deficits. Accumulating evidence suggests a clear correlation between mitochondrial dysfunction and NLRP3 inflammasome activation. Unraveling deeper molecular aspects of mitochondrial dysfunction may provide safer and effective therapeutic alternatives. This review links mitochondrial dysfunction and appraises its role in the pathophysiology of diabetic neuropathy. We have also tried to delineate the role of mitophagy in NLRP3 inflammasome activation in experimental diabetic neuropathy.

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来源期刊

Mitochondrion 生物-细胞生物学

CiteScore

9.40

自引率

4.50%

发文量

审稿时长

13.6 weeks

期刊介绍： Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.