Cited by 393Inflammasome and immune disordersImmune Response and InflammationCell death mechanisms and regulation

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Mitochondria: diversity in the regulation of the NLRP3 inflammasome

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Gurung, Prajwal, Lukens, John R., Kanneganti, Thirumala-Devi·2015·Trends in Molecular Medicine

DOI 10.1016/j.molmed.2014.11.008PMC PMC4352396

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Abstract

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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Authors: Gurung, P., Lukens, J. R., & Kanneganti, T.-D.
Affiliations: St. Jude Children's Research Hospital (US)
ORCID: Gurung, Prajwal
Lukens, John R.
Kanneganti, Thirumala-Devi
Venue: Trends in Molecular Medicine
Publisher: Elsevier BV
Published: 2015-03
Volume: 21
Issue: 3
Pages: 193-201
ISSN: 1471-4914 (ISSN-L)
DOI: 10.1016/j.molmed.2014.11.008
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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Mitochondria: diversity in the regulation of the NLRP3 inflammasome

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