{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T15:18:11Z","timestamp":1790090291948,"version":"4.0.1"},"reference-count":21,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2018,10,9]],"date-time":"2018-10-09T00:00:00Z","timestamp":1539043200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Key Project of Natural Science Foundation of Heilongjiang Province of China","award":["ZD2017015"],"award-info":[{"award-number":["ZD2017015"]}]},{"name":"Yu Weihan Outstanding Youth Training Fund of Harbin Medical University"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2018,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiac hypertrophy is a compensatory response to mechanical stimuli and neurohormonal factors, ultimately progresses to heart failure. The proteins of some transient receptor potential (<jats:styled-content style=\"fixed-case\">TRP<\/jats:styled-content>) channels, Ca<jats:sup>2+<\/jats:sup>\u2010permeable nonselective cation channel, are highly expressed in cardiomyocytes, and associated with the occurrence of cardiac hypertrophy. Transient receptor potential vanilloid 3 (<jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3) is a member of <jats:styled-content style=\"fixed-case\">TRP<\/jats:styled-content>, however, the functional role of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 in cardiac hypertrophy remains unclear. <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 was elevated in pathological cardiac hypertrophy, but not in swimming exercise\u2010induced physiological cardiac hypertrophy in rats. <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 expression was also increased in Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2013induced cardiomyocyte hypertrophy in\u00a0vitro, which was remarkably increased by carvacrol (a nonselective <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content> channel agonist), and reduced by ruthenium red (a nonselective <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content> channel antagonist). Interestingly, we found that activated <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 in Ang <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2013induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated Ca<jats:styled-content style=\"fixed-case\">MKII<\/jats:styled-content> protein expression, and enhancing <jats:styled-content style=\"fixed-case\">NFAT<\/jats:styled-content>c3 nuclear translocation. However, blocking or knockdown of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 could inhibit the expressions of calcineurin, phosphorylated Ca<jats:styled-content style=\"fixed-case\">MKII<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NFAT<\/jats:styled-content>c3 protein by Western blot. In conclusion, the activation of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 aggravated pathological cardiac hypertrophy through calcineurin\/<jats:styled-content style=\"fixed-case\">NFAT<\/jats:styled-content>c3 signalling pathway and correlated with the protein expression levels of calcineurin, phosphorylated Ca<jats:styled-content style=\"fixed-case\">MKII<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NFAT<\/jats:styled-content>c3, revealing that <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>3 might be a potential therapeutic target for cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/jcmm.13880","type":"journal-article","created":{"date-parts":[[2018,10,9]],"date-time":"2018-10-09T18:33:00Z","timestamp":1539109980000},"page":"6055-6067","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Activation of transient receptor potential vanilloid 3 channel (<scp>TRPV<\/scp>3) aggravated pathological cardiac hypertrophy via calcineurin\/<scp>NFAT<\/scp>c3 pathway in rats"],"prefix":"10.1111","volume":"22","author":[{"given":"Qianhui","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pharmacology Harbin Medical University\u2010Daqing Daqing Heilongjiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanping","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Harbin Medical University\u2010Daqing Daqing Heilongjiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yonggang","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Harbin Medical University\u2010Daqing Daqing Heilongjiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pilong","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Harbin Medical University\u2010Daqing 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