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We aimed to determine the pathophysiological roles of CLICs in the heart. For this, we analyzed\n                    <jats:italic>CLIC<\/jats:italic>\n                    expression in cardiomyocytes in a mouse transverse aortic constriction (TAC) model to induce cardiac hypertrophy and failure, as well as in ventricular myocytes from patients with dilated cardiomyopathy (DCM) using single\u2010cell RNA\u2010sequencing. Single\u2010ventricular myocytes were isolated from the left ventricular free wall of C57BL\/6J mice after TAC (pre\u2010TAC; Day 3 post\u2010TAC; and Weeks 1, 2, 4, and 8 post\u2010TAC). Gene expression was compared with data from sham controls. In mice,\n                    <jats:italic>CLIC1<\/jats:italic>\n                    and\n                    <jats:italic>CLIC4<\/jats:italic>\n                    expression significantly increased in Day 3 and Weeks 1, 2, and 4 post\u2010TAC.\n                    <jats:italic>CLIC5<\/jats:italic>\n                    expression showed an increase during all phases. Kyoto Encyclopedia of Genes and Genomes pathway analysis for genes associated with\n                    <jats:italic>CLIC1<\/jats:italic>\n                    ,\n                    <jats:italic>CLIC4<\/jats:italic>\n                    , and\n                    <jats:italic>CLIC5<\/jats:italic>\n                    revealed a strong association between focal adhesion activation and actin cytoskeleton regulation pathways linked to extracellular matrix (ECM) remodeling.\n                    <jats:italic>CLIC1<\/jats:italic>\n                    and\n                    <jats:italic>CLIC4<\/jats:italic>\n                    expression was also higher in cells from patients with DCM. Single\u2010cell RNA\u2010sequencing revealed the possible role of CLICs in myocardial ventricular remodeling linked to ECM, proposing their potential as therapeutic targets for cardiac hypertrophy and failure.\n                  <\/jats:p>","DOI":"10.14814\/phy2.70726","type":"journal-article","created":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T04:29:37Z","timestamp":1768192177000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Implication of intracellular chloride channel in extracellular matrix remodeling in pressure\u2010overloaded mice and patients with dilated cardiomyopathy"],"prefix":"10.14814","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1386-8293","authenticated-orcid":false,"given":"Gaku","family":"Oguri","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine The University of Tokyo  Tokyo 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