Ischaemic diseases such as critical limb ischaemia and myocardial infarction affect millions of people worldwide¹. Transplanting endothelial cells (ECs) is a promising therapy in vascular medicine, but engrafting ECs typically necessitates co-transplanting perivascular supporting cells such as mesenchymal stromal cells (MSCs), which makes clinical implementation complicated^2,3. The mechanisms that enable MSCs to facilitate EC engraftment remain elusive. Here we show that, under cellular stress, MSCs transfer mitochondria to ECs through tunnelling nanotubes, and that blocking this transfer impairs EC engraftment. We devised a strategy to artificially transplant mitochondria, transiently enhancing EC bioenergetics and enabling them to form functional vessels in ischaemic tissues without the support of MSCs. Notably, exogenous mitochondria did not integrate into the endogenous EC mitochondrial pool, but triggered mitophagy after internalization. Transplanted mitochondria co-localized with autophagosomes, and ablation of the PINK1–Parkin pathway negated the enhanced engraftment ability of ECs. Our findings reveal a mechanism that underlies the effects of mitochondrial transfer between mesenchymal and endothelial cells, and offer potential for a new approach for vascular cell therapy.

严重肢体缺血和心肌梗塞等缺血性疾病影响着全世界数百万人¹。移植内皮细胞 (EC) 是血管医学中一种有前途的疗法，但移植 EC 通常需要共同移植血管周围支持细胞，如间充质基质细胞 (MSC)，这使得临床实施变得复杂^2,3。使间充质干细胞促进内皮细胞植入的机制仍然难以捉摸。在这里，我们发现，在细胞应激下，间充质干细胞通过隧道纳米管将线粒体转移到内皮细胞，而阻断这种转移会损害内皮细胞的植入。我们设计了一种人工移植线粒体的策略，暂时增强 EC 生物能，并使它们能够在缺血组织中形成功能性血管，而无需 MSC 的支持。值得注意的是，外源线粒体并未整合到内源EC线粒体库中，而是在内化后引发线粒体自噬。移植的线粒体与自噬体共定位，PINK1-Parkin 通路的消融抵消了 EC 增强的植入能力。我们的研究结果揭示了间充质细胞和内皮细胞之间线粒体转移影响的机制，并为血管细胞治疗的新方法提供了潜力。