A mitochondrial view of aging, reactive oxygen species and metastatic cancer.
This perspective article highlights the growing evidence placing mitochondria and mitochondrial function at the center of cancer as an age-related disease. The discussion starts from the mitochondrial free radical hypothesis that predicts the involvement of endogenous mitochondrial reactive oxygen species (ROS) in cancer development and summarizes studies demonstrating the impact of the modulation of ROS levels on cancer development and metastasis. Cancer is fundamentally a complex interplay of cell growth, division, metastasis and death- processes connected to mitochondria through energy metabolism. Based on this evidence, therapeutics focused on mitochondrial function and mitochondrial ROS production are an attractive approach to modulating the progression of metastatic cancer and the general improvement of human health span.
Ladiges
Warren
W
Department of Comparative Medicine, University of Washington, Seattle, WA 98195, USA. wladiges@u.washington.edu
Wanagat
Jonathan
J
Preston
Bradley
B
Loeb
Lawrence
L
Rabinovitch
Peter
P
D000375:Aging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D017209:Apoptosis; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009362:Neoplasm Metastasis / Q000473:pathology* / Q000628:therapy; D009369:Neoplasms / Q000473:pathology*; D017382:Reactive Oxygen Species / Q000378:metabolism*
D017382:Reactive Oxygen Species