Volume 9, Issue 4 pp. 462-465
REVIEW

A Mitochondrial view of aging, reactive oxygen species and metastatic cancer

Warren Ladiges

Warren Ladiges

Department of Comparative Medicine, University of Washington, Seattle, WA 98195, USA

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Jonathan Wanagat

Jonathan Wanagat

Department of Medicine, Division of Geriatrics, UCLA, Los Angeles, CA, USA

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Bradley Preston

Bradley Preston

Department of Pathology, University of Washington, Seattle, WA 98195, USA

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Lawrence Loeb

Lawrence Loeb

Department of Pathology, University of Washington, Seattle, WA 98195, USA

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Peter Rabinovitch

Peter Rabinovitch

Department of Pathology, University of Washington, Seattle, WA 98195, USA

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First published: 21 July 2010
Citations: 25
Warren Ladiges, Departments of Comparative Medicine, University of Washington, Seattle, WA 98195, USA. Tel.: +1 206 685 3260; fax: +1 206 685 3006; e-mail: [email protected]

Summary

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.

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