Mitochondrial ROS Signaling in Organismal Homeostasis
Open accessAbstract
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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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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NIX-mediated mitophagy protects against proteinuria-induced tubular cell apoptosis and renal injury
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The link between Mitochondria and Sarcopenia
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- Authors
- Shadel, G. S., & Horvath, T. L.
- Affiliations
- Yale University (US)
- Corresponding author
- Shadel, Gerald S.
- ORCID
- Shadel, Gerald S.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 163
- Issue
- 3
- Pages
- 560-569
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4634671
- 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
- bronze
- doi.org
- Licence
- 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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