Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S Nagar, Punjab, India.
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S Nagar, Punjab, India.
Mitochondrion. 2024 Nov;79:101972. doi: 10.1016/j.mito.2024.101972. Epub 2024 Oct 2.
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.
糖尿病性神经病是糖尿病的一种具有挑战性的并发症，其特征是由于糖尿病中的高血糖导致周围神经损伤。线粒体功能障碍已被报道为导致糖尿病性神经病中神经损伤的关键病理生理因素之一，临床上表现为神经退行性变化，如功能和感觉运动缺陷。越来越多的证据表明，线粒体功能障碍与 NLRP3 炎性体激活之间存在明显的相关性。深入研究线粒体功能障碍的分子方面可能提供更安全有效的治疗选择。本综述将线粒体功能障碍联系起来，并评估其在糖尿病性神经病发病机制中的作用。我们还试图描述自噬在实验性糖尿病性神经病中 NLRP3 炎性体激活中的作用。
