Cited by 2,632Redox biology and oxidative stressMitochondrial Function and PathologyAutophagy in Disease and Therapy

Physiological Roles of Mitochondrial Reactive Oxygen Species

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Sena, Laura A., Chandel, Navdeep S.·2012·Molecular Cell

Abstract

Historically, mitochondrial reactive oxygen species (mROS) were thought to exclusively cause cellular damage and lack a physiological function. Accumulation of ROS and oxidative damage have been linked to multiple pathologies, including neurodegenerative diseases, diabetes, cancer, and premature aging. Thus, mROS were originally envisioned as a necessary evil of oxidative metabolism, a product of an imperfect system. Yet few biological systems possess such flagrant imperfections, thanks to the persistent optimization of evolution, and it appears that oxidative metabolism is no different. More and more evidence suggests that mROS are critical for healthy cell function. In this Review, we discuss this evidence following some background on the generation and regulation of mROS.

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Crossref · 10.1016/j.molcel.2012.09.025

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  • Modest levels of ROS can contribute to cellular proliferation and survival.

    “However, increasing evidence suggests that modest levels of ROS can also contribute to cellular proliferation and survival (Sena and Chandel 2012).”

    From Cellular senescence and its effector programs (2014) · cites this paper as Sena and Chandel 2012

  • At low to moderate levels, ROS act as signaling transducers to activate cancer cell proliferation, migration, invasion, angiogenesis, and drug resistance.

    “At low to moderate levels, ROS act as signaling transducers to activate cancer cell proliferation, migration, invasion, angiogenesis, and drug resistance.2, 6, 7”
  • Mitochondrial ROS regulate metabolic adaptation, differentiation, and proliferation.

    “Recent studies indicate that mitochondrial ROS regulate metabolic adaptation, differentiation and proliferation (Sena and Chandel, 2012).”

    From Mitochondria in the Regulation of Innate and Adaptive Immunity (2015) · cites this paper as Sena and Chandel, 2012

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Authors
Sena, L. A., & Chandel, N. S.
Affiliations
Northwestern University (US)
Corresponding author
Chandel, Navdeep S.
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2012-10
Volume
48
Issue
2
Pages
158-167
ISSN
1097-2765 (ISSN-L)
OpenAlex
W2017275974
Cited by
2,632
References
101
Citations by year
2026: 177 · 2025: 165 · 2024: 159 · 2023: 200 · 2022: 207 · 2021: 254 · 2020: 247 · 2019: 220 · 2018: 202 · 2017: 196 · 2016: 181 · 2015: 176 · 2014: 157 · 2013: 88 · 2012: 2
FWCI
12.07
Type
journal article
Language
en
Open access
Locations
  • Molecular Cell (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (P01HL071643, T32HL076139)
  • National Cancer Institute (R01CA123067)
  • National Institute of Environmental Health Sciences (F30ES019815)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondrial reactive oxygen species, oxidative metabolism, oxidative damage, neurodegenerative diseases, diabetes mellitus, cancer, premature aging
MeSH terms
Aging, Antioxidants, Autophagy, Cell Differentiation, Humans, Immunity, Mitochondria, Reactive Oxygen Species, Oxidative Stress

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