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Updated: Feb 1, 2026

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Mitophagy imbalance in cardiomyocyte ischaemia/reperfusion injury
Yu-Zhen Li1, Xu-Dong Wu2, Xiu-Hua Liu1
1Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, China.
Abstract:
The rhythmic contraction of cardiomyocytes consumes a lot of energy. 90% of ATP in cardiomyocytes is produced by mitochondria. Maintenance of a healthy population of mitochondria by mitophagy is critical for cardiomyocyte survival and normal function. Mitophagy refers to selective removal of damaged mitochondria by autophagy mechanism. The process of mitophagy must be restricted to dysfunctional mitochondria and maintained at a balanced level. Disruption in the balance inevitably leads to cardiomyocyte injury and dysfunction. Accumulating evidence suggests that mitophagy plays a pivotal role in ischaemia/reperfusion-induced cardiomyocyte injury. In this review, we focus on the current understanding of mitophgy in cardiomyocyte function, the implications for cardiomyocyte injury in response to ischaemia/reperfusion as well as their underlying potential mechanisms.
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