Mitochondrial therapeutics for cardioprotection
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Updated: May 31, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Raquel S Carreira1, Pamela Lee, Roberta A Gottlieb
1BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, USA.
Abstract:
Mitochondria represent approximately one-third of the mass of the heart and play a critical role in maintaining cellular function-however, they are also a potent source of free radicals and pro-apoptotic factors. As such, maintaining mitochondrial homeostasis is essential to cell survival. As the dominant source of ATP, continuous quality control is mandatory to ensure their ongoing optimal function. Mitochondrial quality control is accomplished by the dynamic interplay of fusion, fission, autophagy, and mitochondrial biogenesis. This review examines these processes in the heart and considers their role in the context of ischemia-reperfusion injury. Interventions that modulate mitochondrial turnover, including pharmacologic agents, exercise, and caloric restriction are discussed as a means to improve mitochondrial quality control, ameliorate cardiovascular dysfunction, and enhance longevity.
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