An extracellular vesicle-mediated mitochondrial transfer network critical for testosterone synthesis.

Kai Xia, Suyuan Zhang, Hao Peng, Hainan Chen, Cuifeng Yang, Jiajie Yu, Peng Luo, Qiying Lu, Hong Chen, Li Huang, Yifei Xiong, Lerong Zhao, Lei Jia, Lu Li, Yuan Qiu, Yan Guo, Congyuan Liu, Hang Fan, Ziran Dai, Guihua Liu, Qiong Ke, Tao Wang, Weiqiang Li, Lili Chen, Chunhua Deng, Haipeng Xiao, Andy Peng Xiang

Department of Urology and Andrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.Department of Urology and Andrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. · pubmed

Paper

Abstract

Testosterone production by testicular Leydig cells (LCs) in male mammals is energetically demanding and prone to mitochondrial damage. Despite these challenges, LCs exhibit remarkable longevity and minimal turnover, suggesting the existence of specialized mechanisms that maintain LC mitochondrial homeostasis under such constrains. Here we identify a mitochondrial transfer network between LCs and different testicular macrophage (tMac) subpopulations. Leydig cells release extracellular vesicles containing defective mitochondria, which are eliminated by CD206

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Research summary

The paper claims that Leydig cells utilize an extracellular vesicle-mediated mitochondrial transfer network to maintain mitochondrial homeostasis for testosterone synthesis. This research is relevant as it explores mechanisms that could contribute to cellular longevity and mitochondrial health, which are critical factors in the aging process.

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