Abstract
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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
