{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:46:54Z","timestamp":1790401614752,"version":"4.1.0"},"reference-count":69,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Podocyte injury is the hallmark of proteinuric kidney diseases, such as FSGS and minimal change disease, and destabilization of the podocyte\u2019s actin cytoskeleton contributes to podocyte dysfunction in many of these conditions. Although agents, such as glucocorticoids and cyclosporin, stabilize the actin cytoskeleton, systemic toxicity hinders chronic use. We previously showed that loss of the kidney-enriched zinc finger transcription factor Kr\u00fcppel-like factor 15 (KLF15) increases susceptibility to proteinuric kidney disease and attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We induced podocyte-specific\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      in two proteinuric murine models, HIV-1 transgenic (\n                      <jats:italic toggle=\"yes\">Tg26<\/jats:italic>\n                      ) mice and adriamycin (ADR)-induced nephropathy, and used RNA sequencing of isolated glomeruli and subsequent enrichment analysis to investigate pathways mediated by podocyte-specific\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      in\n                      <jats:italic toggle=\"yes\">Tg26<\/jats:italic>\n                      mice. We also explored in cultured human podocytes the potential mediating role of Wilms Tumor 1 (WT1), a transcription factor critical for podocyte differentiation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In\n                      <jats:italic toggle=\"yes\">Tg26<\/jats:italic>\n                      mice, inducing podocyte-specific\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      attenuated podocyte injury, glomerulosclerosis, tubulointerstitial fibrosis, and inflammation, while improving renal function and overall survival; it also attenuated podocyte injury in ADR-treated mice. Enrichment analysis of RNA sequencing from the\n                      <jats:italic toggle=\"yes\">Tg26<\/jats:italic>\n                      mouse model shows that\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      induction activates pathways involved in stabilization of actin cytoskeleton, focal adhesion, and podocyte differentiation. Transcription factor enrichment analysis, with further experimental validation, suggests that KLF15 activity is in part mediated by WT1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Inducing podocyte-specific\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      attenuates kidney injury by directly and indirectly upregulating genes critical for podocyte differentiation, suggesting that\n                      <jats:italic toggle=\"yes\">KLF15<\/jats:italic>\n                      induction might be a potential strategy for treating proteinuric kidney disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2018030324","type":"journal-article","created":{"date-parts":[[2018,8,24]],"date-time":"2018-08-24T08:55:41Z","timestamp":1535100941000},"page":"2529-2545","source":"Crossref","is-referenced-by-count":53,"title":["Podocyte-Specific Induction of Kr\u00fcppel-Like Factor 15 Restores Differentiation Markers and Attenuates Kidney Injury in Proteinuric Kidney Disease"],"prefix":"10.1681","volume":"29","author":[{"given":"Yiqing","family":"Guo","sequence":"first","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jesse","family":"Pace","sequence":"additional","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengzhe","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Avi","family":"Ma\u2019ayan","sequence":"additional","affiliation":[{"name":"Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1415-1286","authenticated-orcid":false,"given":"Zichen","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monica P.","family":"Revelo","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Utah, Salt Lake City, Utah;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangchen","family":"Gu","sequence":"additional","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"Attalah","sequence":"additional","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaqi","family":"Yang","sequence":"additional","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chelsea","family":"Estrada","sequence":"additional","affiliation":[{"name":"Nephrology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincent W.","family":"Yang","sequence":"additional","affiliation":[{"name":"Gastroenterology, Department of Medicine, Stony Brook University, Stony Brook, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"He","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine and"},{"name":"Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, Icahn School of Medicine at Mount Sinai, New York, New York;"},{"name":"Renal Section, James J. 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