Advanced glycation end products promote the release of endothelial cell-derived mitocytosis.

Accumulation of advanced glycation end products (AGEs) and endothelial dysfunction are major factors that contribute to the progression of vascular complications in diabetes. Migrasomes, a newly discovered organelle involved in mitocytosis, play an important role in the selective removal of damaged mitochondria. Our research shows that human umbilical vein endothelial cells (HUVECs) can release migrasomes and undergo mitocytosis. In addition, when exposed to oxidative stress from AGEs, mitochondrial damage worsens, leading to the activation of migrasome-mediated mitocytosis. We also found that migrasomes carrying mitochondria can be taken up by recipient cells. Understanding the connection between migrasome release, mitocytosis, and mitochondrial function in endothelial cells sheds light on the biological processes behind intercellular communication.