ArticleEMBO reports2022
CCDC50 suppresses NLRP3 inflammasome activity by mediating autophagic degradation of NLRP3.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- CCDC50 Alleviates Cerebral Ischemia-Reperfusion Injury via Enhancing Autophagy to Inhibit STING/IRF3-Mediated Microglial Polarization.Molecular neurobiology · 2026Article
- Integrated selection scans and cis-eQTL analyses reveal genes and variants associated with milk quality, immunity, and adaptation in endangered Dengchuan cattle.BMC genomics · 2026Article
- Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases.Apoptosis : an international journal on programmed cell death · 2026Article
- Article
- Lactucopicrin promotes the autophagic degradation of MAP2K4/MKK4 by mediating CCDC50 palmitoylation to alleviate osteoarthritis progression.Autophagy · 2026Article
- Natural Products Modulate Plaque Macrophage Functional Programs in Atherosclerosis.Drug design, development and therapy · 2026Review
- Genome-Wide Aggregated Trans-Effects Analysis Implicates Deficient Type III Interferon Signaling as a Key Cause of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2025Article
- Rapid and accurate detection of infectious SARS-CoV-2 by viral receptor capture combined with loop-mediated isothermal amplification.Virologica Sinica · 2025Article
- VANGL2 alleviates inflammatory bowel disease by recruiting the ubiquitin ligase MARCH8 to limit NLRP3 inflammasome activation through OPTN-mediated selective autophagy.PLoS biology · 2025Article
- The PGAM5-NEK7 interaction is a therapeutic target for NLRP3 inflammasome activation in colitis.Acta pharmaceutica Sinica. B · 2025Article
- Implication of the LRR Domain in the Regulation and Activation of the NLRP3 Inflammasome.Cells · 2024Review
- Exposing kinetic disparities between inflammasome readouts using time-resolved analysis.Heliyon · 2024Article
- GSNOR negatively regulates the NLRP3 inflammasome via S-nitrosation of MAPK14.Cellular & molecular immunology · 2024Article
- The Neglected Sibling: NLRP2 Inflammasome in the Nervous System.Aging and disease · 2024Review
- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
- Sirtuin 1 activator alleviated lethal inflammatory injuryFrontiers in pharmacology · 2023Article
- Article
- The role of the NLRP3 inflammasome in chronic inflammation in asthma and chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- CCDC50 suppresses NLRP3 inflammasome activity by mediating autophagic degradation of NLRP3.EMBO reports · 2022Article
- Deciphering the role of autophagy in the immunopathogenesis of inflammatory bowel disease.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRP3-directed inflammasome complex is crucial for the host to resist microbial infection and monitor cellular damage. However, the hyperactivation of NLRP3 inflammasome is implicated in pathogenesis of inflammatory diseases, including inflammatory bowel disease (IBD). Autophagy and autophagy-related genes are closely linked to NLRP3-mediated inflammation in these inflammatory disorders. Here, we report that CCDC50, a novel autophagy cargo receptor, negatively regulates NLRP3 inflammasome assembly and suppresses the cleavage of pro-caspase-1 and interleukin 1β (IL-1β) release by delivering NLRP3 for autophagic degradation. Transcriptome analysis showed that knockdown of CCDC50 results in upregulation of signaling pathways associated with autoinflammatory diseases. CCDC50 deficiency leads to enhanced proinflammatory cytokine response triggered by a wide range of endogenous and exogenous NLRP3 stimuli. Ccdc50-deficient mice are more susceptible to dextran sulfate (DSS)-induced colitis and exhibit more severe gut inflammation with elevated NLRP3 inflammasome activity. These results illustrate the physiological significance of CCDC50 in the pathogenicity of inflammatory diseases, suggesting protective roles of CCDC50 in keeping gut inflammation under control.
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Registered trials
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.