{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T00:12:08Z","timestamp":1788567128083,"version":"build-2803163510"},"reference-count":54,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2018,3,30]],"date-time":"2018-03-30T00:00:00Z","timestamp":1522368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Nantong scientific program","award":["MS22016027"],"award-info":[{"award-number":["MS22016027"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>Cardiovascular and renal inflammation induced by Aldosterone (Aldo) plays a pivotal role in the pathogenesis of hypertension and renal fibrosis. GSK\u20103\u03b2 contributes to inflammatory cardiovascular and renal diseases, but its role in Aldo\u2010induced hypertension, and renal damage is not clear. In the present study, rats were treated with Aldo combined with SB\u2010216763 (a GSK\u20103\u03b2 inhibitor) for 4 weeks. Hemodynamic, cardiac, and renal parameters were assayed at the indicated time. Here we found that rats treated with Aldo presented cardiac and renal hypertrophy and dysfunction. Cardiac and renal expression levels of molecular markers attesting inflammation and fibrosis were increased by Aldo infusion, whereas the treatment of SB\u2010216763 reversed these alterations. SB\u2010216763 suppressed cardiac and renal inflammatory cytokines levels (TNF\u2010a, IL\u20101\u03b2, and MCP\u20101). Meanwhile, SB\u2010216763 increased the protein levels of LC3\u2010II in the cardiorenal tissues as well as p62 degradation, indicating that SB\u2010216763 induced autophagy activation in cardiac, and renal tissues. Importantly, inhibition of autophagy by 3\u2010MA attenuated the role of SB\u2010216763 in inhibiting perivascular fibrosis, and tubulointerstitial injury. These data suggest that SB\u2010216763 protected against Aldo\u2010induced cardiac and renal injury by activating autophagy, and might be a therapeutic option for salt\u2010sensitive hypertension and renal fibrosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcb.26788","type":"journal-article","created":{"date-parts":[[2018,3,30]],"date-time":"2018-03-30T04:09:22Z","timestamp":1522382962000},"page":"5934-5943","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["SB\u2010216763, a GSK\u20103\u03b2 inhibitor, protects against aldosterone\u2010induced cardiac, and renal injury by activating autophagy"],"prefix":"10.1002","volume":"119","author":[{"given":"Yi\u2010De","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Nephrology Affiliated Hospital of Nantong University Nantong Jiangsu 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