review · Metabolism Open
Diabetic nephropathy represents the most frequent complication arising from diabetes mellitus, contributing significantly to long-term illness. While programmed cell death processes such as apoptosis, autophagy, and necroptosis have established roles in the development of kidney damage, ferroptosis has received far less scrutiny. Ferroptosis is a distinct, non-apoptotic form of regulated cell death that relies on iron and is characterised by the accumulation of intracellular lipid peroxides to fatal concentrations. Evidence links ferroptosis directly to kidney cell damage in this condition. Examining the biological mechanisms that drive ferroptosis in diabetic nephropathy helps clarify disease progression and highlights emerging therapeutic targets aimed at preventing or mitigating renal injury.
Diabetic nephropathy is a widespread complication that damages kidneys in people with diabetes. Understanding ferroptosis, a specific form of cell death driven by iron and toxic fat accumulation, provides fresh insight into how kidney cells are destroyed. Clarifying these biological pathways is an essential step towards identifying new medical strategies to preserve kidney function and protect patient health.
Therapeutic targeting of ferroptosis presents opportunities for pharmaceutical developers seeking new treatments for diabetic kidney damage. Because the work focuses on mechanisms and emerging therapeutic concepts, it reflects early-stage research rather than applied products. Any clinical applications or drug discoveries targeting these pathways remain at an exploratory distance from real-world medical practice.
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Diabetic Nephropathy (DN), the most common complication in diabetes mellitus, has been affecting the lives of people diabetic for a long time. Numerous studies have demonstrated the unbreakable connection between ferroptosis and kidney cell damage. Ferroptosis is a type of iron-dependent, non-apoptotic, regulated cell death, characterized by the buildup of intracellular lipid peroxides to lethal levels. Although the role of programmed cell deaths like apoptosis, autophagy, and necroptosis in the pathogenesis of DN has been demonstrated, the implication of ferroptosis in DN was least interrogated. Hence, the main aim of this review was to discuss the current understanding of ferroptosis focusing on its potential mechanisms, its involvement in DN, and emerging therapeutic opportunities.
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DOI: 10.1016/j.metop.2023.100243
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