Mitochondria as a centrally positioned hub in the innate immune response
Open accessAbstract
Mitochondria are vital organelles involved in numerous cellular functions ranging from energy metabolism to cell survival. Emerging evidence suggests that mitochondria provide a platform for signaling pathways involved in innate immune response. Mitochondrial ROS (mtROS) production, mitochondrial DNA (mtDNA) release, mitochondrial antiviral signaling protein (MAVS) are key triggers in the activation of innate immune response following variety of stress signals that include infection, tissue damage and metabolic dysregulation. The process is mediated through pattern recognition receptors (PRRs) that consist of retinoic acid inducible gene like receptors (RLRs), c-type lectin receptors (CLRs), toll type receptors (TLRs) and nuclear oligomerization-domain like receptors (NLRs). These signals converge to form a multiprotein complex called inflammasome that leads to caspase-1 activation to promote processing of precursor cytokines (pro-IL1β and pro-IL-18) to active cytokines (IL-1β and IL-18). It appears that mitochondria induced inflammasome activation contributes to inflammatory process in many diverse disorders. Therefore, strategies aimed at modulating mitochondria mediated inflammasome activation might be beneficial in many pathophysiological conditions. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.
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Cardiolipin, N-formylated peptides, mtDNA, ATP and reactive oxygen species are known mitochondrial damage-associated molecular patterns.
“Cardiolipin, N-formylated peptides, mtDNA, ATP and reactive oxygen species are known mitochondrial damage-associated molecular patterns (9, 28–30).”
From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [30]
The Introduction describes mitochondrial ROS and mtDNA as products released during mitochondrial dysfunction, and section 1.3 explicitly lists ATP as a DAMP. Section 1.1 links cardiolipin to inflammasome activation, but does not call it a DAMP; no passage found identifies N-formylated peptides. The paper therefore supports parts of the list, not the claim that all five are known mitochondrial DAMPs. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMitochondria and their components, such as N-formylated peptides and mtDNA, are recognized as damage-associated molecular patterns that activate innate immunity and elicit inflammation.
“Mitochondria and their components (e.g. N-formylated peptides and mtDNA) are recognized as damage-associated molecular patterns (DAMPs), which activate the innate immune system and elicit an inflammatory response6,21–23.”
From Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations (2019) · cites this paper as [23]
The Introduction and Conclusions (page numbers unavailable) say that released mtDNA activates the NLRP3 inflammasome and that mitochondrial triggers produce an innate inflammatory response. The paper discusses DAMPs, but the passages found do not identify N-formylated peptides as one of them; a search for “formylated” found no such passage. (LLM, conf=0.85)
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- Authors
- Sandhir, R., Halder, A., & Sunkaria, A.
- Affiliations
- Panjab University (IN)
- Corresponding author
- Sandhir, Rajat
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2017-05
- Volume
- 1863
- Issue
- 5
- Pages
- 1090-1097
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2544056465
- Cited by
- 135
- References
- 114
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 20 · 2023: 20 · 2022: 13 · 2021: 13 · 2020: 22 · 2019: 15 · 2018: 12 · 2017: 7
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University Grants Commission, New Delhi (F.4-7/2015/DRS-I(SAP-II))
- Department of Science & Technology, Govt of India
- 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 › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- mitochondria, innate immunity, mitochondrial reactive oxygen species, mitochondrial DNA release, MAVS, pattern recognition receptors, inflammasome, caspase-1, IL-1β, IL-18, Toll-like receptors, C-type lectin receptors, NLRP3 inflammasome, inflammation, mitochondrial signaling
- MeSH terms
- Animals, Humans, Immunity, Innate, Mitochondria, Protein Precursors, Reactive Oxygen Species, Caspase 1, Interleukin-18, Receptors, Pattern Recognition, Interleukin-1beta, Inflammasomes
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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