Mitochondrial dysfunction and oxidative stress in heart disease

• Authors: Jessica N. Peoples, Emory University; Anita Saraf, Emory University; Nasab Ghazal, Emory University; Tyler T. Pham, Emory University; Jennifer Kwong, Emory University
• Journal Title: Experimental and Molecular Medicine
• Volume: Volume 51, Number 12
• Publisher: Springer Nature [academic journals on nature.com]: Fully open access journals | 2019-12-19, Pages 1-13
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1038/s12276-019-0355-7
• Subjects: Chemistry, Biochemistry; Health Sciences, Medicine and Surgery
• Keywords: Science & Technology; Life Sciences & Biomedicine; Biochemistry & Molecular Biology; Medicine, Research & Experimental; Research & Experimental Medicine; PERMEABILITY TRANSITION PORE; CA-2&-INDUCED MEMBRANE TRANSITION; OXYGEN SPECIES GENERATION; VITAMIN-E CONSUMPTION; MYOCARDIAL-INFARCTION; N-ACETYLCYSTEINE; REPERFUSION INJURY; DIABETIC HEART; BETA-CAROTENE; LIFE-SPAN

Abstract

Beyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated process driving oxidative stress and disease pathology, contemporary studies reveal that ROS also facilitate normal physiology. Mitochondria are especially abundant in cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Moreover, there is growing appreciation that medical therapies designed to mediate mitochondrial ROS production can be important strategies to ameliorate cardiac disease. In this review, we highlight evidence from animal models that illustrates the strong connections between mitochondrial ROS and cardiac disease, discuss advancements in the development of mitochondria-targeted antioxidant therapies, and identify challenges faced in bringing such therapies into the clinic.