{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T20:47:26Z","timestamp":1790110046652,"version":"4.0.1"},"reference-count":31,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,4,18]],"date-time":"2013-04-18T00:00:00Z","timestamp":1366243200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p>Fibroblast growth factors (<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gfs) are pleiotropic proteins involved in development, repair and metabolism. <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> is predominantly expressed in the heart. However, as the heart function is essentially normal in <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> knockout mice, its role has remained unclear. To elucidate the pathophysiological role of <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16 in the heart, we examined angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010induced cardiac hypertrophy and fibrosis in <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> knockout mice. Angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010induced cardiac hypertrophy and fibrosis were significantly promoted by enhancing <jats:italic><jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>gf\u2010\u03b2<\/jats:italic><jats:sub><jats:italic>1<\/jats:italic><\/jats:sub> expression in <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> knockout mice. Unexpectedly, the response to cardiac remodeling was apparently opposite to that in <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2<\/jats:italic> knockout mice. These results indicate that <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16 probably prevents cardiac remodeling, although <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2 promotes it. Cardiac <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> expression was induced after the induction of <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2<\/jats:italic> expression by angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>. In cultured cardiomyocytes, <jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16<\/jats:italic> expression was promoted by <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2. In addition, <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16 antagonized <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2\u2010induced <jats:italic><jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>gf\u2010\u03b2<\/jats:italic><jats:sub><jats:italic>1<\/jats:italic><\/jats:sub> expression in cultured cardiomyocytes and noncardiomyocytes. These results suggest a possible mechanism whereby <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf16 prevents angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\u2010induced cardiac hypertrophy and fibrosis by antagonizing <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf2. The present findings should provide new insights into the roles of <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>gf signaling in cardiac remodeling.<\/jats:p>","DOI":"10.1111\/gtc.12055","type":"journal-article","created":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T02:59:21Z","timestamp":1366340361000},"page":"544-553","source":"Crossref","is-referenced-by-count":57,"title":["Angiotensin <scp>II<\/scp>\u2010induced cardiac hypertrophy and fibrosis are promoted in mice lacking <i><scp>F<\/scp>gf16<\/i>"],"prefix":"10.1111","volume":"18","author":[{"given":"Emi","family":"Matsumoto","sequence":"first","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sayaka","family":"Sasaki","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideyuki","family":"Kinoshita","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takuya","family":"Kito","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroya","family":"Ohta","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morichika","family":"Konishi","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koichiro","family":"Kuwahara","sequence":"additional","affiliation":[{"name":"Department of Medicine and Clinical Science Kyoto University Graduate School of Medicine Sakyo Kyoto 606\u20108507 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuwa","family":"Nakao","sequence":"additional","affiliation":[{"name":"Department of Medicine and Clinical Science Kyoto University Graduate School of Medicine Sakyo Kyoto 606\u20108507 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuyuki","family":"Itoh","sequence":"additional","affiliation":[{"name":"Department of Genetic Biochemistry Kyoto University Graduate School of Pharmaceutical Sciences Sakyo Kyoto 606\u20108501 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,4,18]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2792"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00434.2006"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI31044"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.76.6.927"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.2174\/138920208786847917"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/abbi.1998.0967"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms11020407"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1210\/me.2010-0142"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.21681"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.21726"},{"key":"e_1_2_6_12_1","first-page":"143","article-title":"Fibroblast Growth Factor 2 Mediates Isoproterenol\u2010induced Cardiac Hypertrophy through Activation of the Extracellular Regulated Kinase","volume":"2","author":"House S.L.","year":"2010","journal-title":"Mol. 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