{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T04:13:22Z","timestamp":1793938402646,"version":"4.8.0"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T00:00:00Z","timestamp":1758499200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100010903","name":"Key Programme","doi-asserted-by":"crossref","award":["2022YFC2505400"],"award-info":[{"award-number":["2022YFC2505400"]}],"id":[{"id":"10.13039\/501100010903","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81871709"],"award-info":[{"award-number":["81871709"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100022963","name":"Key Research and Development Program of Zhejiang Province","doi-asserted-by":"crossref","award":["LZ23H050001"],"award-info":[{"award-number":["LZ23H050001"]}],"id":[{"id":"10.13039\/100022963","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100022963","name":"Key Research and Development Program of Zhejiang Province","doi-asserted-by":"crossref","award":["LY25H200018"],"award-info":[{"award-number":["LY25H200018"]}],"id":[{"id":"10.13039\/100022963","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Upregulation of Bmpr2 was identified as a central cause of glomerular endothelial cell activation and injury in lupus nephritis.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Glomerular endothelial cells with elevated Bmpr2 expression promoted inflammatory differentiation of macrophages.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>C5a mediated the increase in Bmpr2 expression in glomerular endothelial cells.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Lupus nephritis, a severe complication of SLE, is closely associated with the abnormal activation of glomerular endothelial cells. Despite its significance, the core mechanisms underlying glomerular endothelial cell activation remain elusive.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We performed single-nucleus RNA sequencing (snRNA-seq) on kidney tissues from lupus nephritis patients and mouse models to investigate transcriptional alterations in glomerular endothelial cells and validated our findings in two lupus nephritis models: pristane-induced lupus nephritis and murphy roths large\/\n                      <jats:italic toggle=\"yes\">lpr<\/jats:italic>\n                      mice. Genetically modified mice and cultured cells were used to further validate the key discoveries.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      was identified as a critical regulator, showing significant upregulation in glomerular endothelial cells from both lupus nephritis patients and mouse models. Elevated\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      expression correlated with enhanced glomerular endothelial cell proliferation and migration and increased expression of adhesion molecules (Vcam1, Icam1). BMPR2 activated SMA- and MAD-related proteins-dependent pathways, leading to the upregulation of downstream targets ID1 and ID3, thereby promoting glomerular endothelial cell hyperactivation.\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      overexpression amplified glomerular endothelial cell proliferation and migration, whereas inhibition of inhibitor of DNA binding signaling by 4-[6-[4-[2-(4-Morpholinyl)ethoxy]phenyl]pyrazolo[1,5-a]pyrimidin-3-yl]quinoline (DMH2) or endothelial-specific\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      knockout attenuated these effects. Moreover, targeting BMPR2 signaling reduced the infiltration of\n                      <jats:italic toggle=\"yes\">CD86<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      macrophages into lupus nephritis kidneys. Coculture experiments confirmed that\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      -activated glomerular endothelial cells promoted macrophage differentiation into an inflammatory phenotype. Complement component C5a was identified as a critical upstream inducer of\n                      <jats:italic toggle=\"yes\">Bmpr2<\/jats:italic>\n                      in glomerular endothelial cells, and inhibition of C5a signaling with the C5aR1 antagonist PMX-53 effectively suppressed Bmpr2 upregulation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings highlight BMPR2 as a key regulator of glomerular endothelial cell injury and macrophage-mediated inflammation in lupus nephritis. Targeting BMPR2 or its upstream activators, such as C5a, effectively treated and improved lupus nephritis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000000856","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T16:03:57Z","timestamp":1758557037000},"page":"504-521","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Bmpr2 Drives Aberrant Activation and Injury of Glomerular Endothelial Cells in Lupus Nephritis"],"prefix":"10.1681","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6146-3389","authenticated-orcid":false,"given":"Jianbo","family":"Qing","sequence":"first","affiliation":[{"name":"Department of Nephrology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiejun","family":"Wen","sequence":"additional","affiliation":[{"name":"Pediatric Translational Medicine Institute, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China"},{"name":"Shanghai Children's Medical Center, Pediatric Translationa Medcine Institute, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Wang","sequence":"additional","affiliation":[{"name":"Core Laboratory, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-0521-3759","authenticated-orcid":false,"given":"Yiting","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 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