{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,28]],"date-time":"2026-02-28T22:30:02Z","timestamp":1772317802460,"version":"3.50.1"},"reference-count":19,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2018,6,20]],"date-time":"2018-06-20T00:00:00Z","timestamp":1529452800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81571844"],"award-info":[{"award-number":["81571844"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>The mechanism of transition from chronic pressure overload\u2010induced cardiac hypertrophy to heart failure is still unclear. Angiotensin II (Ang II) may be an important factor that mediates the transition in the end\u2010stage of cardiac hypertrophy. In the present study, Goldblatt two\u2010kidney one\u2010clip (2K1C) rat model was used to simulate Ang II\u2010induced hypertension. The elevated Ang II not only induced the concentric hypertrophy of left ventricle and cardiac fibrosis, but also increased the expression and glycosylation of CD147 in 2K1C rats. The left ventricular structure and function detected by echocardiogram showed a sign of the transition from cardiac hypertrophy to heart failure in 16 weeks of 2K1C rats. Ang II can activate N\u2010acetylglucosamine transferase V (GnT\u2010V), a key enzyme for CD147 glycosylation. Retinoic acid, an agonist of GnT\u2010V, further increased glycosylated CD147, and activated matrix metalloproteinase\u20102\/\u20109 (MMP\u20102 and MMP\u20109) in the hypertrophied left ventricle of 2K1C rat. Meanwhile, collagen cross\u2010linking in the hypertrophied left ventricle significantly reduced in 2K1C rats. On the contrary, tunicamycin, an inhibitor of N\u2010glycan biosynthesis, inhibited glycosylation of CD147 and activity of MMP\u20102 and MMP\u20109, and then maintained a stable of collagen cross\u2010linking in the 2K1C rat hearts. The above results suggested that Ang II increased glycosylated CD147 which activated MMP\u20102 and MMP\u20109. Collagens were degraded by the activated MMPs and then reduced collagen cross\u2010linking. Finally, the hypertrophied left ventricle was progressively dilated in chronic pressure overload due to losing the limitation of collagen cross\u2010linking. Therefore, the compensated hypertrophy of left ventricle gradually transited to congestive heart failure.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26713","type":"journal-article","created":{"date-parts":[[2018,1,29]],"date-time":"2018-01-29T22:13:07Z","timestamp":1517263987000},"page":"8022-8034","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Glycosylated CD147 reduces myocardial collagen cross\u2010linking in cardiac hypertrophy"],"prefix":"10.1002","volume":"119","author":[{"given":"Ning\u2010Yu","family":"Ru","sequence":"first","affiliation":[{"name":"Department of Aerospace Physiology Fourth Military Medical University Xi'an China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Long\u2010Biao","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Aerospace Physiology Fourth Military Medical University Xi'an China"},{"name":"School of Medical Psychology Fourth Military 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