{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["BTMU-FAH","First Affiliated Hospital of Baotou Medical College"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJEB92196"],"long_description":["This study aims to elucidate the role of the NLRP3 inflammasome in regulating the formation of neutrophil extracellular traps (NETs) during rheumatoid arthritis (RA) progression and to evaluate the therapeutic potential of inhibiting NLRP3 or Gasdermin D (GSDMD) in alleviating RA pathology. Neutrophils and synovial tissues were obtained from RA and osteoarthritis (OA) patients, and the expression levels of NLRP3, GSDMD, and NET-related markers were assessed by immunofluorescence, Western blot, and qPCR. A collagen-induced arthritis (CIA) mouse model was used to investigate the effects of inhibiting NLRP3 and GSDMD on joint swelling, bone destruction, and synovial inflammation. Transcriptomic sequencing identified 12 core genes associated with heat shock proteins and histones that exhibited significant differential expression following the inhibition of GSDMD pore formation. Further experiments revealed that NLRP3 activation enhances NET release by promoting the cleavage of GSDMD (generating the active N-terminal fragment), whereas inhibiting NLRP3 or GSDMD effectively blocks this process and markedly improves joint inflammation and tissue damage. In summary, the NLRP3 inflammasome plays a pivotal role in RA pathogenesis by regulating GSDMD-dependent NETosis, and targeting this pathway may offer a novel therapeutic avenue for RA."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Analysis of GSDMD-N Abnormality Promoting Neutrophil NETs-Mediated RA Disease through NLRP3-Dependent Pathway","description":"GSDMD-N Abnormality Promoting Neutrophil NETs-Mediated RA Disease","dates":{"last_updated":"2025-07-09","first_public":"2025-07-09"},"accession":"PRJEB92196","cross_references":{}}