| Literature DB >> 34019840 |
Kevin M Tharp1, Ryo Higuchi-Sanabria2, Greg A Timblin3, Breanna Ford4, Carlos Garzon-Coral5, Catherine Schneider6, Jonathon M Muncie1, Connor Stashko1, Joseph R Daniele7, Andrew S Moore8, Phillip A Frankino2, Stefan Homentcovschi2, Sagar S Manoli9, Hao Shao10, Alicia L Richards11, Kuei-Ho Chen11, Johanna Ten Hoeve12, Gregory M Ku13, Marc Hellerstein6, Daniel K Nomura4, Karou Saijo3, Jason Gestwicki10, Alexander R Dunn14, Nevan J Krogan11, Danielle L Swaney11, Andrew Dillin2, Valerie M Weaver15.
Abstract
Mitochondria control eukaryotic cell fate by producing the energy needed to support life and the signals required to execute programed cell death. The biochemical milieu is known to affect mitochondrial function and contribute to the dysfunctional mitochondrial phenotypes implicated in cancer and the morbidities of aging. However, the physical characteristics of the extracellular matrix are also altered in cancerous and aging tissues. Here, we demonstrate that cells sense the physical properties of the extracellular matrix and activate a mitochondrial stress response that adaptively tunes mitochondrial function via solute carrier family 9 member A1-dependent ion exchange and heat shock factor 1-dependent transcription. Overall, our data indicate that adhesion-mediated mechanosignaling may play an unappreciated role in the altered mitochondrial functions observed in aging and cancer. Published by Elsevier Inc.Entities:
Keywords: UPRmt; adhesion; aging; cancer; extracellular matrix; mechanical stress; mechanotabolism; metabolism; oxidative stress; tension
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Year: 2021 PMID： 34019840 PMCID： PMC8266765 DOI： 10.1016/j.cmet.2021.04.017
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 31.373