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

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

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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Crossref · 10.1016/j.molmed.2014.11.008

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  • Mitochondria is a central regulator of NLRP3 inflammasome activation through ROS, Ca2+, decrease of NAD+, Mfn or mitochondrial DNA.

    “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).”
  • The release of danger signals from mitochondria promotes the formation of inflammasomes.

    “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).”
  • Mitochondria are a central regulator of NLRP3 inflammasome activation through ROS, Ca2+, decrease of NAD+, Mfn or mitochondrial DNA.

    “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).”

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Research works printed but not linked: 2

  1. [37]Chinopoulos C Adam-Vizi V Mitochondrial Ca2+ sequestration and precipitation revisited The FEBS journal 2010 277 18 3637 51 20659160
  2. [59]Nakahira K Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome Nat Immunol 2011 12 3 222 30 21151103 PMC3079381

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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)
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 · 2013: 1
FWCI
2.48
Type
journal article
Language
en
Open access
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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