Iron-mediated lysosomal-mitochondrial crosstalk:a new direction in the treatment of aging and aging-related diseases

• 来源期刊: 生物化学与生物物理学报（英文版）
• 年，卷（期）: 2020,（11）
• 所属期刊栏目: Research Highlights
• 页码范围: 1293-1295
• 页数: 3页
• 语种: 英文

摘要

A recent study by Hughes et al.[1]showed that cysteine-mediated iron deficiency is the main cause of aging-related mitochon-drial dysfunction.They also uncovered that aging-induced vacuo-lar/lysosomal de-acidification participates in the cysteine-mediated iron deficiency,implying that the de-acidifying lysosome triggers vacuolar/lysosomal dysfunction and iron deficiency,further lead-ing to mitochondrial dysfunction.Previous studies showed that iron and lysosomal-mitochondrial crosstalk are the two important mechanisms that lysosome regulates aging,and it is well known that iron plays a pivotal role in various cell metabolic activities[2,3].Accumulating evidence shows that there is a close rela-tionship between lysosome and mitochondria,yet little is known about the exact role of them.The discovery that iron defi-ciency mediates lysosomal-mitochondrial crosstalk has presented a new therapeutic avenue for managing aging and aging-related diseases.