<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zou HM</submitter><funding>Natural Science Foundation of Guizhou Province</funding><funding>National Natural Science Foundation of China</funding><funding>Science and Technology Foundation of Guizhou Provincial Health Commission</funding><funding>National Natural Science Foundation of China’s (NSFC) Cultivation Project</funding><pagination>e001349</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11603702</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) 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.&lt;h4>Methods&lt;/h4>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-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small int</pubmed_abstract><journal>Lupus science &amp; medicine</journal><pubmed_title>HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis.</pubmed_title><pmcid>PMC11603702</pmcid><funding_grant_id>82360147</funding_grant_id><funding_grant_id>gyfynsfc[2022]-53</funding_grant_id><funding_grant_id>QianKeHeJiChu-ZK[2022] General 378</funding_grant_id><funding_grant_id>gzwkj2023-209</funding_grant_id><funding_grant_id>82460148</funding_grant_id><funding_grant_id>QianKeHeJiChu-ZK[2022] General 409</funding_grant_id><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Zou HM</pubmed_authors><pubmed_authors>Xie Y</pubmed_authors><pubmed_authors>Shi MJ</pubmed_authors><pubmed_authors>Liu M</pubmed_authors><pubmed_authors>Luo YQ</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>An XM</pubmed_authors><pubmed_authors>Xu LF</pubmed_authors><pubmed_authors>Chen PL</pubmed_authors><pubmed_authors>Guo B</pubmed_authors><pubmed_authors>Ruan YY</pubmed_authors></additional><is_claimable>false</is_claimable><name>HNF-1β alleviates podocyte injury in lupus nephritis by maintaining endoplasmic reticulum homeostasis.</name><description>&lt;h4>Objective&lt;/h4>The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) 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.&lt;h4>Methods&lt;/h4>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-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small int</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2025-04-19T04:22:25.35Z</modification><creation>2025-04-19T04:22:25.35Z</creation></dates><accession>S-EPMC11603702</accession><cross_references><pubmed>39608815</pubmed><doi>10.1136/lupus-2024-001349</doi></cross_references></HashMap>