{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T19:57:22Z","timestamp":1786132642604,"version":"build-2736575974"},"reference-count":67,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","funder":[{"DOI":"10.13039\/501100008665","name":"Osaka Medical Research Foundation for Intractable Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100008665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK083294"],"award-info":[{"award-number":["DK083294"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK093269"],"award-info":[{"award-number":["DK093269"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000005","name":"Department of Defense","doi-asserted-by":"publisher","award":["W81XWH-17-1-0662"],"award-info":[{"award-number":["W81XWH-17-1-0662"]}],"id":[{"id":"10.13039\/100000005","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      The amelioration of proteinuria resulting from inhibition of the renin-angiotensin pathway is thought to be predominantly caused by reduction in intraglomerular pressure. However, because studies have produced conflicting findings, whether podocyte-associated angiotensin II receptor signaling directly contributes to podocyte injury remains unclear. Angiotensin II receptor type 1 (AT1R) is internalized by clathrin- and dynamin-mediated endocytosis, and in this study the authors used podocyte-specific\n                      <jats:italic toggle=\"yes\">Dynamin 1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">2<\/jats:italic>\n                      double-knockout mice to examine the effect of angiotensin II stimulation on AT1R in these double-knockout mice. Loss of AT1R internalization accentuated Rac1 activation and membrane ruffling in\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout podocytes. Podocyte-specific deletion of the receptor in\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout mice demonstrated improved albuminuria and kidney function and attenuation of membrane abnormalities\u2014findings suggesting that podocyte-associated AT1R signaling augments podocyte injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Inhibition of the renin-angiotensin system remains a cornerstone in reducing proteinuria and progression of kidney failure, effects believed to be the result of reduction in BP and glomerular hyperfiltration. However, studies have yielded conflicting results on whether podocyte-specific angiotensin II (AngII) signaling directly induces podocyte injury. Previous research has found that after AngII stimulation,\n                      <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                      -arrestin\u2013bound angiotensin II receptor type 1 (AT1R) is internalized in a clathrin- and dynamin-dependent manner, and that\n                      <jats:italic toggle=\"yes\">Dynamin1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Dynamin2<\/jats:italic>\n                      double-knockout mice exhibit impaired clathrin-mediated endocytosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used podocyte-specific\n                      <jats:italic toggle=\"yes\">Dyn<\/jats:italic>\n                      double-knockout mice to examine AngII-stimulated AT1R internalization and signaling in primary podocytes and controls. We also examined the\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      effect of AngII in these double-knockout mice through renin-angiotensin system blockers and through deletion of\n                      <jats:italic toggle=\"yes\">Agtr1a<\/jats:italic>\n                      (which encodes the predominant AT1R isoform expressed in kidney, AT1aR). We tested calcium influx, Rac1 activation, and lamellipodial extension in control and primary podocytes of\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout mice treated with AngII.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We confirmed augmented AngII-stimulated AT1R signaling in primary\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout podocytes resulting from arrest of clathrin-coated pit turnover. Genetic ablation of podocyte\n                      <jats:italic toggle=\"yes\">Agtr1a<\/jats:italic>\n                      in\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout mice demonstrated improved albuminuria and kidney function compared with the double-knockout mice. Isolation of podocytes from\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout mice revealed abnormal membrane dynamics, with increased Rac1 activation and lamellipodial extension, which was attenuated in\n                      <jats:italic toggle=\"yes\">Dnm<\/jats:italic>\n                      double-knockout podocytes lacking AT1aR.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results indicate that inhibiting aberrant podocyte-associated AT1aR signaling pathways has a protective effect in maintaining the integrity of the glomerular filtration barrier.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019010053","type":"journal-article","created":{"date-parts":[[2019,9,11]],"date-time":"2019-09-11T14:55:14Z","timestamp":1568213714000},"page":"2307-2320","source":"Crossref","is-referenced-by-count":18,"title":["Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury"],"prefix":"10.1681","volume":"30","author":[{"given":"Kazunori","family":"Inoue","sequence":"first","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuefei","family":"Tian","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heino","family":"Velazquez","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keita","family":"Soda","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhen","family":"Wang","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher E.","family":"Pedigo","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wang","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Cross","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4292-4426","authenticated-orcid":false,"given":"Marwin","family":"Groener","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jee-Won","family":"Shin","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hossam","family":"Hassan","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichi","family":"Yamamoto","sequence":"additional","affiliation":[{"name":"Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; 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