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Podocytes now appear to be a possible direct target in LN in addition to being prone to collateral damage from glomerular capillary lesions induces by immune complexes and inflammatory processes. The NLRP3 inflammasome is regulated by CCAAT\/enhancer\u2010binding protein \u03b2 (C\/EBP\u03b2), which is involved in the pathogenesis of SLE. However, the role and mechanism of C\/EBP\u03b2 in LN remain unclear. In this investigation, glomerular podocytes treated with LN serum and MRL\/lpr mice were employed as <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic> models of LN, respectively. <jats:italic>In vivo<\/jats:italic>, the expression of C\/EBP\u03b2 isoforms was detected in kidney specimens of humans and mice with LN. Then we assessed the effect of C\/EBP\u03b2 inhibition on renal structure and function by injecting RNAi adeno\u2010associated virus of C\/EBP\u03b2 shRNA into MRL\/lpr mice. <jats:italic>In vitro<\/jats:italic>, glomerular podocytes were treated with LN serum and C\/EBP\u03b2 siRNA to explore the role of C\/EBP\u03b2 in the activation of the AIM2 inflammasome and podocyte injury. C\/EBP\u03b2\u2010LAP and C\/EBP\u03b2\u2010LIP were significantly overexpressed in kidney tissue samples from LN patients and mice, and C\/EBP\u03b2 inhibition significantly alleviated renal function damage and ameliorated renal structural deficiencies. Inflammatory pathways downstream from the AIM2 inflammasome could be suppressed by C\/EBP\u03b2 knockdown. Furthermore, the upregulation of C\/EBP\u03b2\u2010LAP could activate the AIM2 inflammasome and podocyte pyroptosis by binding to the promoters of <jats:italic>AIM2<\/jats:italic> and <jats:italic>CASPASE1<\/jats:italic> to enhance their expression, and the knockdown of AIM2 or (and) caspase\u20101 reversed the effects of C\/EBP\u03b2\u2010LAP overexpression. Interestingly, C\/EBP\u03b2\u2010LIP overexpression could transcriptionally inhibit IRAG and promote Ca<jats:sup>2+<\/jats:sup> release\u2010mediated activation of the AIM2 inflammasome. This finding suggests that C\/EBP\u03b2 is not only involved in the regulation of the expression of key proteins of the AIM2 inflammasome but also affects the polymerization of key proteins of the AIM2 inflammasome through the regulation of Ca<jats:sup>2+<\/jats:sup> release. In conclusion, this study provides a new idea for studying the regulatory mechanism of C\/EBP\u03b2 and provides a theoretical basis for the early diagnosis and treatment of LN in the future. \u00a9 2023 The Pathological Society of Great Britain and Ireland.<\/jats:p>","DOI":"10.1002\/path.6174","type":"journal-article","created":{"date-parts":[[2023,8,21]],"date-time":"2023-08-21T21:42:23Z","timestamp":1692654143000},"page":"269-285","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["<scp>C<\/scp>\/<scp>EBP\u03b2<\/scp> isoform\u2010specific regulation of podocyte pyroptosis in lupus nephritis\u2010induced renal injury"],"prefix":"10.1002","volume":"261","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4867-4402","authenticated-orcid":false,"given":"Huimei","family":"Zou","sequence":"first","affiliation":[{"name":"Department of Pathophysiology Guizhou Medical University  Guiyang PR China"},{"name":"Guizhou 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