ArticleCell death & disease2024
HECTD3 inhibits NLRP3 inflammasome assembly and activation by blocking NLRP3-NEK7 interaction.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 13 citations in OpenAlex.
- Modulation of the gut microbiota by traditional Chinese medicine to attenuate chemotherapy-induced toxicity in gastric cancer: a review.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Review
- Nrf2 promotes NLRP3 inflammasome assembly and activation by Klf9-TXNIP axis.Cell death discovery · 2026Article
- HECT ubiquitin ligases as regulators of inflammatory signalling.Cell death and differentiation · 2026Review
- Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026Review
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Structure and mechanism of the HECT ligase HECTD3.Nature communications · 2026Article
- Anwei decoction alleviates chronic atrophic gastritis by modulating the gut microbiota-metabolite axis andWorld journal of gastroenterology · 2026Article
- NLR inflammasome pathways: key targets for pathogenesis and therapy of metabolic diseases.Frontiers in immunology · 2026Review
- Deciphering the NEK7-NLRP3 inflammasome assembly: from conformational activation to allosteric drug discovery.Frontiers in immunology · 2026Review
- Identifying transcriptomic signatures that mediate the causal effect of genotype on Alzheimer's disease.Frontiers in neuroscience · 2026Article
- The role of NLRP3 inflammasome in necrotizing enterocolitis.Pediatric research · 2026Review
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
- The role of HECT-type E3 ubiquitin ligases in inflammation.Frontiers in immunology · 2026Review
- Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- NLRP3 inflammasome and pyroptosis: implications in inflammation and multisystem disorders.PeerJ · 2025Review
- The role of NLRP3 inflammasome in multiple sclerosis: pathogenesis and pharmacological application.Frontiers in immunology · 2025Review
- Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells.Cell death discovery · 2024Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.