{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:35:36Z","timestamp":1745469336520,"version":"3.40.4"},"reference-count":26,"publisher":"S. Karger AG","issue":"1-2","license":[{"start":{"date-parts":[[2013,2,26]],"date-time":"2013-02-26T00:00:00Z","timestamp":1361836800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2013,2,26]],"date-time":"2013-02-26T00:00:00Z","timestamp":1361836800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron Exp Nephrol"],"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Background\/Aims:&lt;\/i&gt;&lt;\/b&gt; To examine the role of the angiotensin II (ATII) type 1a receptor (AT1-R) pathway in renal tissue damage and repair, we investigated reversible glomerular injury in a mouse model of habu snake venom (HSV)-induced glomerulonephritis using AT1-R-deficient (AT1a-\/-) mice and AT1-R antagonist-treated mice. &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; Experimental glomerulonephritis was induced by single administration of HSV to AT1a+\/+ mice (HSV group) and AT1a-\/- mice (KO-HSV group) and AT1-R antagonist-treated BL6 mice (HSV-ARB group). Morphological change and expression levels of type IV collagen, CD31, and vascular endothelial growth factor (VEGF) were analyzed. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; The HSV group showed increased mesangial matrix expansion on day 7, which returned to preinjection levels by day 56, while mes-angial matrix expansion and increased type IV collagen expression were seen throughout days 7 to 56 in the KO-HSV group. The KO-HSV group showed fewer CD31-positive capillary loops and a marked decrease in the number of VEGF-positive cells in the glomeruli than the HSV group. VEGF administration to the KO-HSV group facilitated glomerular capillary repair and reconstruction. The HSV-ARB group showed the same delay in glomerular repair as that seen in the KO-HSV group. &lt;b&gt;&lt;i&gt;Conclusion:&lt;\/i&gt;&lt;\/b&gt; Our results indicate that blocking of the ATII-AT1R pathway delays glomerular repair via angiogenesis inhibition, followed by reduced induction of VEGF.<\/jats:p>","DOI":"10.1159\/000346954","type":"journal-article","created":{"date-parts":[[2013,2,26]],"date-time":"2013-02-26T09:56:29Z","timestamp":1361872589000},"page":"13-22","source":"Crossref","is-referenced-by-count":3,"title":["Glomerular Repair Retardation via Blocking of Angiotensin II Type 1a Receptor Pathway in a Mouse Glomerulonephritis 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