What can we do to optimize mitochondrial transplantation therapy for myocardial ischemia-reperfusion injury?

Mitochondrial transplantation is a promising solution for the heart following ischemia-reperfusion injury due to its capacity to replace damaged mitochondria and restore cardiac function. However, many barriers (such as inadequate mitochondrial internalization, poor survival of transplanted mitochondria, few mitochondria colocalized with cardiac cells) compromise the replacement of injured mitochondria with transplanted mitochondria. Therefore, it is necessary to optimize mitochondrial transplantation therapy to improve clinical effectiveness. By analogy, myocardial ischemia-reperfusion injury is like a withered flower, it needs to absorb enough nutrients to recover and bloom. In this review, we present a comprehensive overview of nutrients (source of exogenous mitochondria and different techniques for mitochondrial isolation), absorption (mitochondrial transplantation approaches, mitochondrial transplantation dose and internalization mechanism), and flowering (the mechanism of mitochondrial transplantation in cardioprotection) for myocardial ischemia-reperfusion injury.

Automated summary

Mitochondrial transplantation is a promising solution for restoring cardiac function following ischemia-reperfusion injury. However, there are several barriers that need to be overcome. This review provides an overview of the importance of nutrients, mitochondrial transplantation methods, and mechanisms of cardioprotection in myocardial ischemia-reperfusion injury.