Mitochondrial ROS regulation of proliferating cells
Abstract
Once thought of exclusively as damaging molecules, reactive oxygen species (ROS) are becoming increasingly appreciated for the role they play in cellular signaling through redox biology. Notably, mitochondria are a major source of ROS within a cell (mROS). Mounting evidence now clearly shows that mROS are critical for intracellular redox signaling by which they contribute to a plethora of cellular processes such as proliferation. mROS are essential for physiological cell proliferation, particularly by the regulation of hypoxia inducible factors (HIFs) under hypoxia. mROS are also vital mediators of growth factor signaling cascades such as angiotensin II (Ang II) and T-cell receptor (TCR) signaling. Pathological proliferative diseases such as cancer utilize mROS to their advantage, aberrantly activating growth factor signaling cascades and perpetuating angiogenesis under hypoxia. This review discusses how mROS positively regulate mitogenic cellular signaling through redox biology, which is critical for both physiological and pathological proliferation.
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Mitochondrial ROS have been implicated in pathways leading to cell proliferation and senescence and in activation of JNK and NF-κB.
“Additionally, mitochondrial ROS have been implicated in pathways leading to cell proliferation and senescence (233, 1046) as well as in the activation of other major cell signaling molecules such as the MAP kinase JNK and NF-κB (330, 689).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [233]
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- Authors
- Diebold, L., & Chandel, N. S.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Chandel, Navdeep S.
- ORCID
- Chandel, Navdeep S.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2016-11
- Volume
- 100
- Pages
- 86-93
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2347147930
- Cited by
- 391
- References
- 128
- Citations by year
- 2026: 15 · 2025: 26 · 2024: 32 · 2023: 47 · 2022: 47 · 2021: 55 · 2020: 48 · 2019: 51 · 2018: 35 · 2017: 29 · 2016: 6
- FWCI
- 3.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM008061)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- mitochondrial reactive oxygen species, redox signaling, cell proliferation, hypoxia-inducible factor, hypoxia, angiotensin II signaling, T cell receptor signaling, cancer, angiogenesis, growth factor signaling
- MeSH terms
- Animals, Humans, Mitochondria, Signal Transduction, Reactive Oxygen Species, Cell Proliferation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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