{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T13:05:24Z","timestamp":1784293524646,"version":"3.55.0"},"reference-count":30,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,3,1]],"date-time":"2019-03-01T00:00:00Z","timestamp":1551398400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,3,1]],"date-time":"2019-03-01T00:00:00Z","timestamp":1551398400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Advanced glycation end products (AGE) and angiotensin II were closely correlated with the progression of diabetic nephopathy (DN). Nitric oxide (NO) is a protective mediator of renal tubular hypertrophy in DN. Here, we examined the molecular mechanisms of angiotensin\u2010converting enzyme inhibitor (ACEI) and NO signaling responsible for diminishing AGE\u2010induced renal tubular hypertrophy. In human renal proximal tubular cells, AGE decreased NO production, inducible NOS activity, guanosine 3\u2032,5\u2032\u2010cyclic monophosphate (cGMP) synthesis, and cGMP\u2010dependent protein kinase (PKG) activation. All theses effects of AGE were reversed by treatment with ACEIs (captopril and enalapril), the NO donor\n                    <jats:italic>S<\/jats:italic>\n                    \u2010nitroso\u2010\n                    <jats:italic>N<\/jats:italic>\n                    \u2010acetylpenicillamine (SNAP), and the PKG activator 8\u2010\n                    <jats:italic>para<\/jats:italic>\n                    \u2010chlorophenylthio\u2010cGMPs (8\u2010pCPT\u2010cGMPs). In addition, AGE\u2010enhanced activation of extracellular signal\u2010regulated kinase (ERK), c\u2010Jun N\u2010terminal kinase (JNK), and p38 mitogen\u2010activated protein kinase (MAPK) were clearly reduced by captopril, enalapril, SNAP, and 8\u2010pCPT\u2010cGMPs. The abilities of ACEIs and NO\/PKG activation to inhibit AGE\u2010induced hypertrophic growth were verified by the observation that captopril, enalapril, SNAP, and 8\u2010pCPT\u2010cGMPs decreased protein levels of fibronectin, p21\n                    <jats:sup>Waf1\/Cip1<\/jats:sup>\n                    , and receptor for AGE. The results of the present study suggest that ACEIs significantly reduced AGE\u2010increased ERK\/JNK\/p38 MAPK activation and renal tubular hypertrophy partly through enhancement of the NO\/PKG pathway.\n                  <\/jats:p>","DOI":"10.1002\/jcp.28369","type":"journal-article","created":{"date-parts":[[2019,3,2]],"date-time":"2019-03-02T00:46:23Z","timestamp":1551487583000},"page":"17473-17481","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Angiotensin\u2010converting enzyme inhibitors attenuated advanced glycation end products\u2010induced renal tubular hypertrophy via enhancing nitric oxide signaling"],"prefix":"10.1002","volume":"234","author":[{"given":"Jean\u2010Yu","family":"Hwang","sequence":"first","affiliation":[{"name":"Department of Food Nutrition Chung Hwa University of Medical Technology Tainan Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei\u2010Chih","family":"Kan","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Division of Nephology, Chi\u2010Mei Medical Center Tainan Taiwan, ROC"},{"name":"Department of Medical Laboratory Science and Biotechnology Chung Hwa University of Medical Technology Tainan Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao\u2010Bin","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medical Laboratory Science and Biotechnology Chung Hwa University of Medical Technology Tainan Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lea\u2010Yea","family":"Chuang","sequence":"additional","affiliation":[{"name":"Department of Biochemistry Kaohsiung Medical University Kaohsiung Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinn\u2010Yuh","family":"Guh","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Kaohsiung Medical University Kaohsiung Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu\u2010Lin","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Medical Laboratory Science and Biotechnology Chung Hwa University of Medical Technology Tainan Taiwan, ROC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1171-6958","authenticated-orcid":false,"given":"Jau\u2010Shyang","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Medical Laboratory Science and Biotechnology Chung Hwa University of Medical Technology Tainan Taiwan, 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