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<p>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<sup>hi</sup> tMacs in a TREM2-dependent process. Deletion of <i>Trem2</i> in tMacs disrupts this transfer, leading to impaired testosterone synthesis. Conversely, LCs acquire extracellular vesicles containing functional mitochondria from MHCII<sup>hi</sup> tMacs through ITGβ1–VCAM1 interactions. Loss of <i>Vcam1</i> in LCs hinders this mitochondrial transfer, thereby compromising testosterone production. Together, our findings reveal an unrecognized mitochondrial transfer network between LCs and tMacs that safeguards LC homeostasis and testosterone production, offering valuable insights into intercellular communication mechanisms that maintain tissue homeostasis.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月27日

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  • 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

摘要

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 CD206hi tMacs in a TREM2-dependent process. Deletion of Trem2 in tMacs disrupts this transfer, leading to impaired testosterone synthesis. Conversely, LCs acquire extracellular vesicles containing functional mitochondria from MHCIIhi tMacs through ITGβ1–VCAM1 interactions. Loss of Vcam1 in LCs hinders this mitochondrial transfer, thereby compromising testosterone production. Together, our findings reveal an unrecognized mitochondrial transfer network between LCs and tMacs that safeguards LC homeostasis and testosterone production, offering valuable insights into intercellular communication mechanisms that maintain tissue homeostasis.