{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T14:22:40Z","timestamp":1787062960282,"version":"build-2736575974"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2025,9,2]],"date-time":"2025-09-02T00:00:00Z","timestamp":1756771200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK112984, DK121846"],"award-info":[{"award-number":["DK112984, DK121846"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000738","name":"US Department of Veterans Affairs","doi-asserted-by":"crossref","award":["1I01BX003698, 1I01BX005300"],"award-info":[{"award-number":["1I01BX003698, 1I01BX005300"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000738","name":"US Department of Veterans Affairs","doi-asserted-by":"crossref","award":["5IK2BX005380"],"award-info":[{"award-number":["5IK2BX005380"]}],"id":[{"id":"10.13039\/100000738","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100015502","name":"Dialysis Clinics","doi-asserted-by":"crossref","award":["DCI"],"award-info":[{"award-number":["DCI"]}],"id":[{"id":"10.13039\/100015502","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100015502","name":"Dialysis Clinics","doi-asserted-by":"crossref","award":["DCI"],"award-info":[{"award-number":["DCI"]}],"id":[{"id":"10.13039\/100015502","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":"\n Key Points<\/jats:title>\n \n \n \n Detrimental effects of Kr\u00fcppel-like factor 4 knockdown in podocytes were eliminated with the inhibition of signal transducer and activator of transcription 3 (STAT3) signaling specifically in podocytes.<\/jats:p>\n <\/jats:list-item>\n \n Human kidney biopsies with renal vasculitis demonstrated a glomerular enrichment of STAT3 downstream genes, which negatively correlated with eGFR.<\/jats:p>\n <\/jats:list-item>\n \n Deconvolution of the bulk RNA-seq from Nephrotic Syndrome Study Network showed an enrichment of STAT3 downstream genes in podocytes as compared with other cell clusters.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n \n Podocyte loss and parietal epithelial cell activation are features of subtypes of glomerulonephritis and FSGS. We recently reported that the podocyte-specific loss of\n Kr\u00fcppel-like factor 4<\/jats:italic>\n (\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n ) triggers dysregulated glomerular signal transducer and activator of transcription 3 (STAT3) activation, podocyte loss with parietal epithelial cell activation and proliferation, leading to FSGS. Although pharmacologic systemic STAT3 inhibition attenuated this phenotype, it remains unclear whether the detrimental effects of\n Klf4<\/jats:italic>\n loss are primarily a result of dysregulated STAT3 activation intrinsically in podocytes.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Mice with the concurrent and conditional knockdown of\n Stat3<\/jats:italic>\n and\n Klf4<\/jats:italic>\n (\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n Stat3<\/jats:italic>\n \u0394Pod<\/jats:sup>\n ) were generated and characterized. Expression arrays from kidney biopsies with various types of glomerular diseases, deposited in Nephroseq, were interrogated for glomerular expression of genes downstream of STAT3 signaling. Cell-specific modulation of STAT3 genes was determined using single-cell RNA sequencing\u2013based proportional cell type deconvolution of bulk RNA-seq obtained from the Nephrotic Syndrome Study Network (NEPTUNE) FSGS and healthy controls.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n Stat3<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice demonstrated no significant podocyte loss, parietal epithelial cell activation and proliferation, FSGS lesions, albuminuria, kidney dysfunction, and tubulointerstitial fibrosis and inflammation compared with the\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice.\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n Stat3<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice also exhibited less glomerular myofibroblasts (+\n \u03b1<\/jats:italic>\n -smooth muscle actin) as compared with\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice. Overall survival was restored in\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n Stat3<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice as compared with\n Klf4<\/jats:italic>\n \u0394Pod<\/jats:sup>\n mice. Interrogation of expression arrays from human kidney biopsies with renal vasculitis demonstrated a glomerular enrichment of genes involved in canonical STAT3 signaling as compared with healthy controls, which negatively correlated with eGFR. Deconvolution of the bulk RNA-seq data from NEPTUNE showed an enrichment of these STAT3 genes in podocytes as compared with other glomerular cell clusters.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Collectively, these data demonstrate that inhibiting podocyte-specific STAT3 signaling was sufficient to counter the detrimental effects of\n Klf4<\/jats:italic>\n loss in podocytes and prevented albuminuria, accelerated podocyte loss, activation and proliferation of parietal epithelial cells, FSGS lesions, and kidney failure.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.0000000841","type":"journal-article","created":{"date-parts":[[2025,8,29]],"date-time":"2025-08-29T16:02:03Z","timestamp":1756483323000},"page":"490-503","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":2,"title":["Podocyte-Specific Deletion of STAT3 in Kr\u00fcppel-Like Factor 4\u2013Related Experimental Podocytopathy"],"prefix":"10.1681","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-3705-3221","authenticated-orcid":false,"given":"Yogesh","family":"Gowthaman","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chelsea C.","family":"Estrada","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"},{"name":"Division of Nephrology, Department of Medicine, Northport Veterans Affairs Medical Center, Northport, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-0417-4588","authenticated-orcid":false,"given":"Joseph","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5437-3433","authenticated-orcid":false,"given":"Yiqing","family":"Guo","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8537-8835","authenticated-orcid":false,"given":"Robert","family":"Bronstein","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3866-3120","authenticated-orcid":false,"given":"David J.","family":"Salant","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1502-2849","authenticated-orcid":false,"given":"John C.","family":"He","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7760-6965","authenticated-orcid":false,"given":"Vivette D.","family":"D\u2019Agati","sequence":"additional","affiliation":[{"name":"Department of Pathology and Cell Biology, Columbia University, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6324-7807","authenticated-orcid":false,"given":"Sandeep K.","family":"Mallipattu","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York"},{"name":"Division of 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