Cited by 1,353Redox biology and oxidative stressMitochondrial Function and PathologyAutophagy in Disease and Therapy

Mitochondrial ROS Signaling in Organismal Homeostasis

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Shadel, Gerald S., Horvath, Tamas L.·2015·Cell

Abstract

Generation, transformation, and utilization of organic molecules in support of cellular differentiation, growth, and maintenance are basic tenets that define life. In eukaryotes, mitochondrial oxygen consumption plays a central role in these processes. During the process of oxidative phosphorylation, mitochondria utilize oxygen to generate ATP from organic fuel molecules but in the process also produce reactive oxygen species (ROS). While ROS have long been appreciated for their damage-promoting, detrimental effects, there is now a greater understanding of their roles as signaling molecules. Here, we review mitochondrial ROS-mediated signaling pathways with an emphasis on how they are involved in various basal and adaptive physiological responses that control organismal homeostasis.

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Crossref · 10.1016/j.cell.2015.10.001

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  • Mitochondria are involved in neuronal redox homeostasis, reactive oxygen species production, calcium buffering, and intracellular signaling.

    “Mitochondria are also involved in neuronal redox homeostasis, reactive oxygen species (ROS) production, calcium buffering, and intracellular signaling [41–44].”

    From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [44]

    The “Mitochondrial ROS Signaling” section describes mitochondrial ROS production and redox signaling, while the brain-focused sections discuss mitochondrial ROS control in neurons. “Mitochondria and Associated Homeostatic and Stress Signaling Pathways” also names ion homeostasis, but the passages do not establish the more specific claim of neuronal calcium buffering. Page numbers were not available in our copy. (LLM, conf=0.85)

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Cited by

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Authors
Shadel, G. S., & Horvath, T. L.
Affiliations
Yale University (US)
Corresponding author
Shadel, Gerald S.
Venue
Cell
Publisher
Elsevier BV
Published
2015-10
Volume
163
Issue
3
Pages
560-569
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2133770419
Cited by
1,353
References
19
Citations by year
2026: 129 · 2025: 170 · 2024: 141 · 2023: 140 · 2022: 155 · 2021: 156 · 2020: 147 · 2019: 95 · 2018: 83 · 2017: 71 · 2016: 61 · 2015: 3
FWCI
7.08
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (R01AG047632, R01AG040236)
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, ROS signaling, oxidative phosphorylation, mitochondrial oxygen consumption, cell differentiation, ATP production
MeSH terms
Animals, Homeostasis, Humans, Mitochondria, Signal Transduction, Exercise, Reactive Oxygen Species

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