IMR Press / FBL / Volume 21 / Issue 6 / DOI: 10.2741/4453

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Role of mitochondrial function in cell death and body metabolism

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1 Severans Biomedical Research Institute and Department of Internal Medicine, Yonsei University College of Medicine, Yonsei-ro Seodaemun-gu, Seoul 03722, Korea
Academic Editors:Yau-Huei Wei, Myung-Shik Lee
Front. Biosci. (Landmark Ed) 2016, 21(6), 1233–1244; https://doi.org/10.2741/4453
Published: 1 June 2016
Abstract

Mitochondria are the key players in apoptosis and necrosis. Mitochondrial DNA (mtDNA)-depleted ρ0 cells were resistant to diverse apoptosis inducers such as TNF-alpha, TNFSF10, staurosporine and p53. Apoptosis resistance was accompanied by the absence of mitochondrial potential loss or cytochrome c translocation. ρ0 cells were also resistant to necrosis induced by reactive oxygen species (ROS) donors due to upregulation of antioxidant enzymes such as manganese superoxide dismutase. Mitochondria also has a close relationship with autophagy that plays a critical role in the turnover of senescent organelles or dysfunctional proteins and may be included in ‘cell death’ category. It was demonstrated that autophagy deficiency in insulin target tissues such as skeletal muscle induces mitochondrial stress response, which leads to the induction of FGF21 as a ‘mitokine’ and affects the whole body metabolism. These results show that mitochondria are not simply the power plants of cells generating ATP, but are closely related to several types of cell death and autophagy. Mitochondria affect various pathophysiological events related to diverse disorders such as cancer, metabolic disorders and aging.

Keywords
Mitochondria
Apoptosis
Cell Death
ROS
Aging
Autophagy
Mitokine
Senescence
Review
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