한빛사논문
Thanh T. Nguyen1,13, Shibo Wei2,13, Thu Ha Nguyen3, Yunju Jo1, Yan Zhang4, Wonyoung Park5, Karim Gariani6, Chang-Myung Oh1, Hyeon Ho Kim7, Ki-Tae Ha5, Kyu Sang Park3, Raekil Park1, In-Kyu Lee 8, Minho Shong9, Riekelt H. Houtkooper10,11,12,* and Dongryeol Ryu1,*
1Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology (GIST), Gwangju 61005, Republic of Korea.
2Department of Precision Medicine, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea.
3Department of Physiology, Yonsei University Wonju College of Medicine, Wonju 26426, Republic of Korea.
4Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea.
5Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
6Service of Endocrinology, Diabetes, Nutrition and Patient Therapeutic Education, Geneva University Hospitals, Geneva 1205, Switzerland.
7Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
8Department of Internal Medicine, School of Medicine, Kyungpook National University, Kyungpook National University Hospital, Daegu 41944, Republic of Korea.
9Department of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea.
10LaboratoryGenetic Metabolic Diseases, Amsterdam UMC Location University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
11Amsterdam Gastroenterology Endocrinology and Metabolism, Amsterdam UMC Location University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. 12Amsterdam Cardiovascular Sciences, Amsterdam UMC Location University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
13These authors contributed equally: Thanh T. Nguyen, Shibo We
*Corresponding author: correspondence to Riekelt H. Houtkooper or Dongryeol Ryu
Abstract
Mitochondria, ubiquitous double-membrane-bound organelles, regulate energy production, support cellular activities, harbor metabolic pathways, and, paradoxically, mediate cell fate. Evidence has shown mitochondria as points of convergence for diverse cell death-inducing pathways that trigger the various mechanisms underlying apoptotic and nonapoptotic programmed cell death. Thus, dysfunctional cellular pathways eventually lead or contribute to various age-related diseases, such as neurodegenerative, cardiovascular and metabolic diseases. Thus, mitochondrion-associated programmed cell death-based treatments show great therapeutic potential, providing novel insights in clinical trials. This review discusses mitochondrial quality control networks with activity triggered by stimuli and that maintain cellular homeostasis via mitohormesis, the mitochondrial unfolded protein response, and mitophagy. The review also presents details on various forms of mitochondria-associated programmed cell death, including apoptosis, necroptosis, ferroptosis, pyroptosis, parthanatos, and paraptosis, and highlights their involvement in age-related disease pathogenesis, collectively suggesting therapeutic directions for further research.
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