| First Author | Xu H | Year | 2025 |
| Journal | Redox Biol | Volume | 79 |
| Pages | 103471 | PubMed ID | 39740362 |
| Mgi Jnum | J:373036 | Mgi Id | MGI:7856094 |
| Doi | 10.1016/j.redox.2024.103471 | Citation | Xu H, et al. (2025) Cardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis. Redox Biol 79:103471 |
| abstractText | Ca(2+) overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca(2+) homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury. We showed that the expression of myocardial Piezo1 was elevated in the infracted area of I/R and cardiomyocyte-specific Piezo1 deficiency (Piezo1( big up tri, openMyh6)) mice attenuated I/R by decreasing infarct size and cardiac dysfunction. Piezo1( big up tri, openMyh6) regulated mitochondrial fusion and fission to improve mitochondrial function and decrease inflammation and oxidative stress in vivo and in vitro. Mechanistically, myocardial Piezo1 knockout alleviated intracellular calcium overload to normalize calpain-associated mitochondrial homeostasis. Our findings indicated that Piezo1 depletion in cardiomyocytes partially restored mitochondrial homeostasis during cardiac ischemia/reperfusion (I/R) injury. This study suggests an innovative therapeutic strategy to alleviate cardiac I/R injury. |
