{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T22:24:35Z","timestamp":1776119075246,"version":"3.50.1"},"reference-count":38,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,6,1]]},"abstract":"<jats:p>Loss of functional nephrons associated with chronic kidney disease induces glomerular hyperfiltration and compensatory renal hypertrophy. We hypothesized that the endothelial nitric oxide synthase (eNOS) [soluble guanylate cyclase (sGC)] protein kinase G (PKG) pathway plays an important role in compensatory renal hypertrophy after unilateral nephrectomy. Analysis of mice subjected to unilateral nephrectomy showed increases in kidney weight-to-body weight and total protein-to-DNA ratios in wild-type but not eNOS knockout (eNOSKO) mice. Serum creatinine and blood urea nitrogen increased after nephrectomy in eNOSKO but not in wild-type mice. Furthermore, Bay 41\u20132272, an sGC stimulator, induced compensatory renal hypertrophy in eNOSKO mice and rescued renal function. The NO donor S-nitrosoglutathione (GSNO) and Bay 41\u20132272 stimulated PKG activity and induced phosphorylation of Akt protein in human proximal tubular cells. GSNO also induced phosphorylation of eukaryotic initiation factor 4E-binding protein and ribosomal protein S6. Our results highlight the importance of the eNOS-NO-PKG pathway in compensatory renal hypertrophy and suggest that reduced eNOS-NO bioavailability due to endothelial dysfunction is the underlying mechanism of failure of compensatory hypertrophy and acceleration of progressive renal dysfunction.<\/jats:p>","DOI":"10.1152\/ajprenal.00459.2011","type":"journal-article","created":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T04:15:15Z","timestamp":1330575315000},"page":"F1402-F1408","source":"Crossref","is-referenced-by-count":32,"title":["Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice"],"prefix":"10.1152","volume":"302","author":[{"given":"Hajime","family":"Nagasu","sequence":"first","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Minoru","family":"Satoh","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan; 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