Mitochondrial control of inflammation
Open accessAbstract
Numerous mitochondrial constituents and metabolic products can function as damage-associated molecular patterns (DAMPs) and promote inflammation when released into the cytosol or extracellular milieu. Several safeguards are normally in place to prevent mitochondria from eliciting detrimental inflammatory reactions, including the autophagic disposal of permeabilized mitochondria. However, when the homeostatic capacity of such systems is exceeded or when such systems are defective, inflammatory reactions elicited by mitochondria can become pathogenic and contribute to the aetiology of human disorders linked to autoreactivity. In addition, inefficient inflammatory pathways induced by mitochondrial DAMPs can be pathogenic as they enable the establishment or progression of infectious and neoplastic disorders. Here we discuss the molecular mechanisms through which mitochondria control inflammatory responses, the cellular pathways that are in place to control mitochondria-driven inflammation and the pathological consequences of dysregulated inflammatory reactions elicited by mitochondrial DAMPs.
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Mitochondria are recognised as damage-associated molecular patterns (DAMPs) that can elicit immune responses.
“Mitochondria are recognised as damage-associated molecular patterns (DAMPs) that can elicit immune responses [4,28].”
From Antimitochondrial antibodies in systemic lupus erythematosus are associated with and predict nephritis, arterial vascular events, and mortality (2026) · cites this paper as [28]
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- Authors
- Marchi, S., Guilbaud, E., Tait, S. W. G., Yamazaki, T., & Galluzzi, L.
- Affiliations
- Marche Polytechnic University (IT)
- Weill Cornell Medicine (US)
- Cancer Research UK Scotland Institute (GB)
- Corresponding author
- Yamazaki, Takahiro
- Galluzzi, Lorenzo
- Venue
- Nature Reviews Immunology
- Published
- 2022-07-25
- Volume
- 23
- Issue
- 3
- Pages
- 159-173
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC9310369
- OpenAlex
- W4287447395
- Cited by
- 1,027
- References
- 218
- Citations by year
- 2026: 250 · 2025: 322 · 2024: 264 · 2023: 171 · 2022: 19
- FWCI
- 20.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Funders
- National Science Foundation
- U.S. Department of Defense (#BC180476P1, #BC210945)
- Cancer Research UK
- Tenovus
- Prostate Cancer UK
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Ministero della Salute (GR‐2016‐02364602)
- National Institutes of Health
- Weill Cornell Medical College
- Stand Up To Cancer (ZP-6177)
- National Cancer Institute (CA274291, U54CA274291)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitochondrial dysfunction, inflammation, damage-associated molecular patterns, mitochondrial membrane permeabilization, mitophagy, autophagy, autoreactivity, autoimmunity, infectious diseases, cancer
- MeSH terms
- Alarmins, Humans, Inflammation, Mitochondria, Neoplasms
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