<p>Ischemic cardiomyopathy (ICM) arises from restricted myocardial blood flow, leading to ischemia/reperfusion (I/R) injury, mitochondrial dysfunction, and heart failure. This commentary highlights the role of mitochondrial homeostasis in cardiac health, emphasizing dysregulated dynamics, ROS production, and mitophagy in ICM and related conditions like diabetic cardiomyopathy. Li et al.‘s study identifies the HOXB5–Sirt5 signaling axis as a key regulator that protects against I/R injury by reducing apoptosis, oxidative stress, ferroptosis, and mitochondrial fragmentation in vitro and in vivo. Future research should explore cell-specific roles and human models to enhance translational potential.</p>

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Mitochondria at the Heart of Ischemia-Reperfusion (I/R) Injury: the HOXB5-Sirt5 Axis

  • Callum J. Quinn,
  • Epiphany S. Velasco,
  • Xander H. T. Wehrens

摘要

Ischemic cardiomyopathy (ICM) arises from restricted myocardial blood flow, leading to ischemia/reperfusion (I/R) injury, mitochondrial dysfunction, and heart failure. This commentary highlights the role of mitochondrial homeostasis in cardiac health, emphasizing dysregulated dynamics, ROS production, and mitophagy in ICM and related conditions like diabetic cardiomyopathy. Li et al.‘s study identifies the HOXB5–Sirt5 signaling axis as a key regulator that protects against I/R injury by reducing apoptosis, oxidative stress, ferroptosis, and mitochondrial fragmentation in vitro and in vivo. Future research should explore cell-specific roles and human models to enhance translational potential.