{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu L"],"funding":["Key Research and Development Program of Shaanxi Province","Health Research and Innovation Capacity Enhancement Program of Shaanxi Province","National Natural Science Foundation of China"],"pagination":["19"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12748425"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["83(1)"],"pubmed_abstract":["Vascular calcification is a pathological process commonly associated with cardiovascular diseases, diabetes, and renal insufficiency, driven by inflammation, oxidative stress, and endoplasmic reticulum stress. IL-38, a member of the IL-1 cytokine family, has shown anti-inflammatory, antioxidant, and anti-fibrotic effects in cardiovascular contexts. However, its role in vascular calcification remains unknown. This study demonstrated significantly reduced IL-38 expression in human calcified coronary tissues, patient plasma, and experimental models. IL-38 knockout mice exhibited aggravated vascular calcification, while treatment with recombinant IL-38 protein markedly suppressed calcification. RNA sequencing revealed that IL-38 alleviates oxidative stress by upregulating glutathione peroxidas"],"journal":["Cellular and molecular life sciences : CMLS"],"pubmed_title":["IL-38 attenuates vascular calcification by upregulating GPX3-mediated antioxidant defense via the PPAR-γ/NRF2 axis."],"pmcid":["PMC12748425"],"funding_grant_id":["2023-ZDLSF-39","82170336","2024TD-05"],"pubmed_authors":["Shang B","Jing L","Cui J","Li P","Liu R","Sun Y","Yi W","Xin J","Wang Q","Zhu L","Cui Y","Chen W","Tang W","Zhang B","Zhou H","Song Y"],"additional_accession":[]},"is_claimable":false,"name":"IL-38 attenuates vascular calcification by upregulating GPX3-mediated antioxidant defense via the PPAR-γ/NRF2 axis.","description":"Vascular calcification is a pathological process commonly associated with cardiovascular diseases, diabetes, and renal insufficiency, driven by inflammation, oxidative stress, and endoplasmic reticulum stress. IL-38, a member of the IL-1 cytokine family, has shown anti-inflammatory, antioxidant, and anti-fibrotic effects in cardiovascular contexts. However, its role in vascular calcification remains unknown. This study demonstrated significantly reduced IL-38 expression in human calcified coronary tissues, patient plasma, and experimental models. IL-38 knockout mice exhibited aggravated vascular calcification, while treatment with recombinant IL-38 protein markedly suppressed calcification. RNA sequencing revealed that IL-38 alleviates oxidative stress by upregulating glutathione peroxidas","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-06T09:31:40.171Z","creation":"2026-05-28T03:12:01.922Z"},"accession":"S-EPMC12748425","cross_references":{"pubmed":["41307654"],"doi":["10.1007/s00018-025-05990-5"]}}