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<p>Post-myocardial infarction remodeling is a major cause of heart failure, with contributions from multiple organs. Brown adipose tissue protects against cardiovascular disease, but the mediators of brown adipose tissue-heart crosstalk and their roles in cardiac remodeling remain elusive. Here, we show that mitochondria-derived vesicles from brown adipose tissue transfer to cardiac macrophages and attenuate pathological remodeling via anti-inflammatory effects. Vesicles containing mitochondrial membranes, rather than mitochondrial matrix, mobilize from brown adipose tissue to the heart in response to stress. VPS35 translocation to mitochondria drives protein packaging into mitochondria-derived vesicles for secretion through extracellular vesicle trafficking machinery. <i>Becn1</i> deficiency impairs VPS35 translocation, alters mitochondria-derived vesicle cargo, and abolishes brown adipose tissue-mediated cardioprotection. Proteomics identifies mitochondrial respiratory chain complex V as a hallmark of protective mitochondria-derived vesicles. These vesicles enhance reparative cytokine production and oxidative phosphorylation rewiring in macrophages. Purified mitochondria-derived vesicles markedly improve remodeling in male mice. Our study uncovers an interorgan transfer of bioenergetic units that contributes to tissue repair.</p>

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Mitochondria-derived vesicles with bioenergetic units from brown adipose tissue attenuate cardiac remodeling post-myocardial infarction

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月21日

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  • Tingting Shi,
  • Feng Chen,
  • Yue Xu,
  • Kai Jiang,
  • Ruhua Deng,
  • Xingbo Yang,
  • Yang Chen,
  • Wenliang Che,
  • John Hwa,
  • Dandan Wang,
  • Yaozu Xiang

摘要

Post-myocardial infarction remodeling is a major cause of heart failure, with contributions from multiple organs. Brown adipose tissue protects against cardiovascular disease, but the mediators of brown adipose tissue-heart crosstalk and their roles in cardiac remodeling remain elusive. Here, we show that mitochondria-derived vesicles from brown adipose tissue transfer to cardiac macrophages and attenuate pathological remodeling via anti-inflammatory effects. Vesicles containing mitochondrial membranes, rather than mitochondrial matrix, mobilize from brown adipose tissue to the heart in response to stress. VPS35 translocation to mitochondria drives protein packaging into mitochondria-derived vesicles for secretion through extracellular vesicle trafficking machinery. Becn1 deficiency impairs VPS35 translocation, alters mitochondria-derived vesicle cargo, and abolishes brown adipose tissue-mediated cardioprotection. Proteomics identifies mitochondrial respiratory chain complex V as a hallmark of protective mitochondria-derived vesicles. These vesicles enhance reparative cytokine production and oxidative phosphorylation rewiring in macrophages. Purified mitochondria-derived vesicles markedly improve remodeling in male mice. Our study uncovers an interorgan transfer of bioenergetic units that contributes to tissue repair.