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However, the effects of TRPV4 on pressure overload-induced cardiac hypertrophy remain unclear. In this study, we found that TRPV4 expression was significantly increased in mouse hypertrophic hearts, human failing hearts, and neurohormone-induced hypertrophic cardiomyocytes. Deletion of TRPV4 attenuated transverse aortic constriction (TAC)-induced cardiac hypertrophy, cardiac dysfunction, fibrosis, inflammation, and the activation of NF\u03baB - NOD - like receptor pyrin domain-containing protein 3 (NLRP3) in mice. Furthermore, the TRPV4 antagonist GSK2193874 (GSK3874) inhibited cardiac remodeling and dysfunction induced by TAC. In vitro, pretreatment with GSK3874 reduced the neurohormone-induced cardiomyocyte hypertrophy and intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration elevation. The specific TRPV4 agonist GSK1016790A (GSK790A) triggered Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx and evoked the phosphorylation of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \/calmodulin-dependent protein kinase II (CaMKII). But these effects were abolished by removing extracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    or GSK3874. More importantly, TAC or neurohormone stimulation-induced CaMKII phosphorylation was significantly blocked by TRPV4 inhibition. Finally, we show that CaMKII inhibition significantly prevented the phosphorylation of NF\u03baB induced by GSK790A. Our results suggest that TRPV4 activation contributes to pressure overload-induced cardiac hypertrophy and dysfunction. This effect is associated with upregulated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \/CaMKII mediated activation of NF\u03baB-NLRP3. Thus, TRPV4 may represent a potential therapeutic drug target for cardiac hypertrophy and dysfunction after pressure overload.\n                  <\/jats:p>","DOI":"10.7554\/elife.74519","type":"journal-article","created":{"date-parts":[[2022,6,6]],"date-time":"2022-06-06T08:15:17Z","timestamp":1654503317000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.74519","source":"Crossref","is-referenced-by-count":34,"title":["Activation of transient receptor potential vanilloid 4 is involved in pressure overload-induced cardiac hypertrophy"],"prefix":"10.7554","volume":"11","author":[{"given":"Yan","family":"Zou","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/048q23a93","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Xuzhou Central Hospital","place":["Xuzhou, China"]},{"id":[{"id":"https:\/\/ror.org\/048q23a93","id-type":"ROR","asserted-by":"publisher"}],"name":"Xuzhou Institute of Cardiovascular Disease, Xuzhou Central Hospital","place":["Xuzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miaomiao","family":"Zhang","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/048q23a93","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Xuzhou Central Hospital","place":["Xuzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiongfeng","family":"Wu","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00p991c53","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning","family":"Zhao","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00p991c53","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minwei","family":"Chen","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00mcjh785","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Xiamen Key Laboratory of Cardiac Electrophysiology, Xiamen Institute of Cardiovascular Diseases, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University","place":["Xiamen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cui","family":"Yang","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00mcjh785","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Xiamen Key Laboratory of Cardiac Electrophysiology, Xiamen Institute of Cardiovascular Diseases, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University","place":["Xiamen, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1125-0294","authenticated-orcid":true,"given":"Yimei","family":"Du","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00p991c53","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology","place":["Wuhan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bing","family":"Han","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/048q23a93","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cardiology, Xuzhou Central Hospital","place":["Xuzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"4374","published-online":{"date-parts":[[2022,6,22]]},"reference":[{"key":"bib1","doi-asserted-by":"publisher","first-page":"269","DOI":"10.1038\/s41569-019-0315-x","article-title":"Reappraising the role of inflammation in heart failure","volume":"17","author":"Adamo","year":"2020","journal-title":"Nature Reviews. 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