Mitochondrial Transplantation Augments the Reparative Capacity of Macrophages Following Myocardial Injury by Yuning Zhang, Xiaolei Sun,* Yawei Jin, Kanghui Chen, Lu Zhang, Xiong Gao, Mohan Li, Ze Yuan, Jianguo Jia, Aijun Sun,* and Junbo Ge* ISBN 10.1002/ADVS.202506337 instant download

Mitochondrial Transplantation Augments the Reparative Capacity of Macrophages Following Myocardial Injury by Yuning Zhang, Xiaolei Sun,* Yawei Jin, Kanghui Chen, Lu Zhang, Xiong Gao, Mohan Li, Ze Yuan, Jianguo Jia, Aijun Sun,* and Junbo Ge* ISBN 10.1002/ADVS.202506337 instant download

The pathologically remodeled myocardial ischemic microenvironment,1. IntroductionCardiovascular disease remains one of thecharacterized by sustained hypoxia, metabolic insufficiency, and accumulationmost significant global health burdens,of inflammatory mediators, severely disrupts mitochondrial homeostasis. Thiswith ischemic heart disease (IHD) beingdysfunction establishes a self-perpetuating cycle that impairs the coordinatedthe leading cause of death among affectedhealing cascade and compromises cardiac tissue repair following myocardialpatients.[1] The immune response plays ainfarction (MI). To counteract these effects, a novel strategy of mitochondrialpivotal role in the progression of myocardial infarction (MI), critically influencingaugmentation is proposed, whereby healthy exogenous mitochondria aredisease outcomes.[2] Among immune cells,introduced into macrophages to generate mitochondria-transplantedmacrophages exhibit remarkable chemotacmacrophages (Mito-T-Macros or MTMs), which can resist post-MI stress.tic and plastic properties, allowing them toMitochondrial transplantation (MT) effectively induces macrophagerapidly respond to stress signals. Throughpolarization toward a reparative M2-like phenotype, thereby enhancingphenotypic transformation, they preciselypro-healing functions, including migration, invasion, and phagocytosis. Inmodulate disease processes and remain oneof the most active cell types at every stagevivo, MTM therapy enhances cardiac function after MI and attenuates leftfollowing MI.[3,4]ventricular remodeling by reducing fibrosis, limiting apoptosis, andThe post-MI ischemic microenvironpromoting angiogenesis. Mechanistically, MT accelerates the phenotypicment is characterized by hypoxia, entransition of macrophages to a reparative state and prolongs their activityergy crisis, oxidative stress, inflammaduring the healing phase. Notably, a portion of the transplanted mitochondriatory responses, and extracellular matrixremodeling, all