{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T04:58:41Z","timestamp":1781585921698,"version":"3.54.5"},"reference-count":53,"publisher":"BMJ","issue":"2","license":[{"start":{"date-parts":[[2024,11,27]],"date-time":"2024-11-27T00:00:00Z","timestamp":1732665600000},"content-version":"unspecified","delay-in-days":26,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100005329","name":"Natural Science Foundation of Guizhou Province","doi-asserted-by":"publisher","award":["QianKeHeJiChu-ZK[2022] General 378"],"award-info":[{"award-number":["QianKeHeJiChu-ZK[2022] General 378"]}],"id":[{"id":"10.13039\/501100005329","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005329","name":"Natural Science Foundation of Guizhou Province","doi-asserted-by":"publisher","award":["QianKeHeJiChu-ZK[2022] General 409"],"award-info":[{"award-number":["QianKeHeJiChu-ZK[2022] General 409"]}],"id":[{"id":"10.13039\/501100005329","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82360147"],"award-info":[{"award-number":["82360147"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82460148"],"award-info":[{"award-number":["82460148"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Science and Technology Foundation of Guizhou Provincial Health Commission","award":["gzwkj2023-209"],"award-info":[{"award-number":["gzwkj2023-209"]}]},{"name":"National Natural Science Foundation of China\u2019s (NSFC) Cultivation Project","award":["gyfynsfc[2022]-53"],"award-info":[{"award-number":["gyfynsfc[2022]-53"]}]}],"content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["Lupus Sci Med"],"accepted":{"date-parts":[[2024,11,8]]},"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-\u03b2) in lupus nephritis (LN) by investigating its modulation of the Derlin-1\/valosin-containing protein (VCP)\/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER) stress and podocyte apoptosis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>In vitro and in vivo models of LN were established using glomerular podocytes treated with LN serum and MRL\/lpr mice, respectively. The expression levels of HNF1-\u03b2 were analysed in kidney tissues from patients with LN and MRL\/lpr mice. To assess the effects of HNF1-\u03b2 inhibition, an adeno-associated virus vector carrying HNF1-\u03b2 short hairpin was administered to MRL\/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-\u03b2 small interfering RNA (siRNA) or HNF1-\u03b2 overexpression plasmids to explore their regulatory effects on the Derlin-1\/VCP\/VIMP complex and podocyte apoptosis. Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were performed to investigate the transcriptional activation of Derlin-1 and VCP promoters by HNF1-\u03b2.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>A significant decrease in HNF1-\u03b2 levels was observed in kidney tissues from patients with LN while MRL\/lpr mice exhibited an initial compensatory increase followed by a subsequent decrease in renal HNF1-\u03b2 expression. Overexpression of HNF1-\u03b2 transcriptionally upregulated Derlin-1 and VCP mitigating LN serum-induced ER stress and podocyte apoptosis. In contrast, HNF1-\u03b2 inhibition exacerbated renal dysfunction and structural damage in MRL\/lpr mice. Interestingly, HNF1-\u03b2 inhibition transcriptionally repressed ERP44, leading to calcium ions (Ca\u00b2<jats:sup>+<\/jats:sup>) release-mediated disruption and inactivation of the Derlin-1\/VCP\/VIMP complex. This finding suggests that HNF1-\u03b2 not only regulates the expression of key proteins in the Derlin-1\/VCP\/VIMP complex but also influences their assembly through Ca\u00b2<jats:sup>+<\/jats:sup> release regulation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>This study provides novel insights into the regulatory mechanisms of HNF1-\u03b2 in LN emphasising its impact on the Derlin-1\/VCP\/VIMP complex, ER stress and podocyte apoptosis. These findings have the potential to inform the development of new diagnostic tools and therapeutic strategies for LN.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/lupus-2024-001349","type":"journal-article","created":{"date-parts":[[2024,11,28]],"date-time":"2024-11-28T04:10:42Z","timestamp":1732767042000},"page":"e001349","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":5,"title":["HNF-1\u03b2 alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis"],"prefix":"10.1136","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4867-4402","authenticated-orcid":false,"given":"Hui-mei","family":"Zou","sequence":"first","affiliation":[{"name":"Department of Pathophysiology, Guizhou Medical University, Guiyang, China"},{"name":"School of Nursing, Guizhou Medical University, Guiyang, 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