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Mitochondria: diversity in the regulation of the NLRP3 inflammasome
Open accessAbstract
Recent studies have identified new roles for mitochondria in the regulation of autoinflammatory processes. Emerging data suggests that the release of danger signals from mitochondria in response to stress and infection promotes the formation of the inflammatory signaling platform known as inflammasomes. Activation of inflammasomes by damaged mitochondria results in caspase-1-dependent secretion of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18, and an inflammatory form of cell death referred to as pyroptosis. Here, we review recently described mechanisms that have been proposed to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation. In addition, we highlight how aberrant regulation of mitochondria-induced inflammasome activation centrally contributes to the inflammatory process that is responsible for obesity and associated metabolic diseases.
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“In fact, mitochondria is considered a central regulator of NLRP3 inflammasome activation through ROS, Ca 2+ , decrease of NAD + , Mfn or mitochondrial DNA (Gurung et al., 2015).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Gurung et al., 2015
In the citing paper
“The release of danger signals from mitochondria promotes the formation of inflammasomes. In fact, mitochondria is considered a central regulator of NLRP3 inflammasome activation through ROS, Ca 2+ , decrease of NAD + , Mfn or mitochondrial DNA (Gurung et al., 2015).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Gurung et al., 2015
In the citing paper
“mitochondria is considered a central regulator of NLRP3 inflammasome activation through ROS, Ca 2+ , decrease of NAD + , Mfn or mitochondrial DNA (Gurung et al., 2015).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Gurung et al., 2015
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Cites
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Cited by
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Molecular mechanisms regulating NLRP3 inflammasome activation
Jo, E.-K., Kim, J. K., Shin, D.-M., & Sasakawa, C. (2016) · Cellular & Molecular Immunology · doi:10.1038/cmi.2015.95 · Cited by 1,378
Reactive oxygen species and mitochondria: A nexus of cellular homeostasis
Dunn, J. D., Álvarez, L., Zhang, X., & Soldati, T. (2015) · Redox Biology · doi:10.1016/j.redox.2015.09.005 · Cited by 1,233
Mitochondria in the Regulation of Innate and Adaptive Immunity
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Common neurodegenerative pathways in obesity, diabetes, and Alzheimer's disease
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Metadata
- Authors
- Gurung, P., Lukens, J. R., & Kanneganti, T.-D.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 21
- Issue
- 3
- Pages
- 193-201
- ISSN
- 1471-4914 (ISSN-L)
- PMC
- PMC4352396
- OpenAlex
- W1999224782
- Cited by
- 393
- References
- 89
- Citations by year
- 2026: 19 · 2025: 26 · 2024: 32 · 2023: 37 · 2022: 28 · 2021: 45 · 2020: 57 · 2019: 37 · 2018: 32 · 2017: 32 · 2016: 33 · 2015: 14
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Lebanese Syrian Associated Charities
- National Institutes of Health
- National Cancer Institute (R01CA163507, CA163507)
- National Institute of Allergy and Infectious Diseases (AI101935, R01AI101935, R37AI101935)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR056296, AR-056296)
- 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 › Cell death mechanisms and regulation
- Keywords
- mitochondria, NLRP3 inflammasome, inflammasome activation, autoinflammation, caspase-1, IL-1β, IL-18, pyroptosis, mitochondrial damage, mitochondrial stress, obesity, metabolic inflammation
- MeSH terms
- Carrier Proteins, Humans, Mitochondria, Models, Biological, Obesity, Reactive Oxygen Species, Inflammasomes
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