ArticleMedComm2023
Vitamin D3 attenuates SARS-CoV-2 nucleocapsid protein-caused hyperinflammation by inactivating the NLRP3 inflammasome through the VDR-BRCC3 signaling pathway in vitro and in vivo.
Article in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Association between vitamin D receptor gene polymorphisms, inflammatory cytokines (IL-1, IL-6, and IL-10), and fracture healing in sports-related injuries.Journal of medical biochemistry · 2025Article
- Vitamin D3 suppresses NLRP3 inflammasome pathway and enhances steroid sensitivity in a neutrophilic steroid hyporesponsive asthma mouse model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Vitamin DFrontiers in nutrition · 2025Article
- NLRP3 Inflammasomes: Dual Function in Infectious Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- Empagliflozin ameliorates vascular calcification in diabetic mice through inhibiting Bhlhe40-dependent NLRP3 inflammasome activation.Acta pharmacologica Sinica · 2024Article
- The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.Biomolecules & biomedicine · 2024Review
- Vitamin D regulates COVID-19 associated severity by suppressing the NLRP3 inflammasome pathway.PloS one · 2024Article
- Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-caused coronavirus disease 2019 (COVID-19) is a global crisis with no satisfactory therapies. Vitamin D3 (VD3) is considered a potential candidate for COVID-19 treatment; however, little information is available regarding the exact effects of VD3 on SARS-CoV-2 infection and the underlying mechanism. Herein, we confirmed that VD3 reduced SARS-CoV-2 nucleocapsid (N) protein-caused hyperinflammation in human bronchial epithelial (HBE) cells. Meanwhile, VD3 inhibited the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation in N protein-overexpressed HBE (HBE-N) cells. Notably, the inhibitors of caspase-1, NLRP3, and
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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.