Cited by 1,014Inflammasome and immune disordersImmune Response and InflammationUbiquitin and proteasome pathways

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Dopamine Controls Systemic Inflammation through Inhibition of NLRP3 Inflammasome

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Yan, Yiqing, Jiang, Wei, Liu, Lei, Wang, Xiaqiong, Ding, Chen, Tian, Zhigang, Zhou, Rongbin·2015·Cell

DOI 10.1016/j.cell.2014.11.047

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Abstract

Inflammasomes are involved in diverse inflammatory diseases, so the activation of inflammasomes needs to be tightly controlled to prevent excessive inflammation. However, the endogenous regulatory mechanisms of inflammasome activation are still unclear. Here, we report that the neurotransmitter dopamine (DA) inhibits NLRP3 inflammasome activation via dopamine D1 receptor (DRD1). DRD1 signaling negatively regulates NLRP3 inflammasome via a second messenger cyclic adenosine monophosphate (cAMP), which binds to NLRP3 and promotes its ubiquitination and degradation via the E3 ubiquitin ligase MARCH7. Importantly, in vivo data show that DA and DRD1 signaling prevent NLRP3 inflammasome-dependent inflammation, including neurotoxin-induced neuroinflammation, LPS-induced systemic inflammation, and monosodium urate crystal (MSU)-induced peritoneal inflammation. Taken together, our results reveal an endogenous mechanism of inflammasome regulation and suggest DRD1 as a potential target for the treatment of NLRP3 inflammasome-driven diseases.

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Authors: Yan, Y., Jiang, W., Liu, L., Wang, X., Ding, C., Tian, Z., & Zhou, R.
Affiliations: University of Science and Technology of China (CN)
Beijing Proteome Research Center (CN)
Corresponding author: Tian, Zhigang
Zhou, Rongbin
ORCID: Yan, Yiqing
Jiang, Wei
Liu, Lei
Wang, Xiaqiong
Ding, Chen
Tian, Zhigang
Zhou, Rongbin
Venue: Cell
Publisher: Elsevier BV
Published: 2015-01
Volume: 160
Issue: 1-2
Pages: 62-73
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2014.11.047
OpenAlex: W2084158898
Cited by: 1,014
References: 49
Citations by year: 2026: 59 · 2025: 93 · 2024: 98 · 2023: 103 · 2022: 108 · 2021: 124 · 2020: 112 · 2019: 79 · 2018: 104 · 2017: 66 · 2016: 47 · 2015: 20
FWCI: 34.32
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 379 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: National Natural Science Foundation of China (81222040, 81330078)
Ministry of Education of the People's Republic of China (20123402110010, 20123402120001)
National Key Research and Development Program of China (2013CB944904, 2014CB910800)
Fundamental Research Funds for the Central Universities
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 › Ubiquitin and proteasome pathways
Keywords: dopamine, NLRP3 inflammasome, dopamine D1 receptor, cAMP signaling, ubiquitination, inflammasome regulation, systemic inflammation, neuroinflammation, lipopolysaccharide-induced inflammation, peritonitis
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Cyclic AMP, Animals, Autophagy, Carrier Proteins, Dopamine, Inflammation, Mice, Inbred C57BL, Receptors, Dopamine, Signal Transduction, Receptors, Dopamine D1, Neurotransmitter Agents, Mice, Ubiquitination, Inflammasomes, Protein Aggregates

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Dopamine Controls Systemic Inflammation through Inhibition of NLRP3 Inflammasome

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