{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T23:18:01Z","timestamp":1791415081978,"version":"4.3.3"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2024,5,21]]},"abstract":"<jats:sec sec-type=\"background\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">S100a8\/9 (S100 calcium binding protein a8\/9) belongs to the S100 family and has gained a lot of interest as a critical regulator of inflammatory response. Our previous study found that S100a8\/9 homolog promoted aortic valve sclerosis in mice with chronic kidney disease. However, the role of S100a8\/9 in pressure overload\u2010induced cardiac hypertrophy remains unclear. The present study was to explore the role of S100a8\/9 in cardiac hypertrophy.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">Cardiomyocyte\u2010specific S100a9 loss or gain of function was achieved using an adeno\u2010associated virus system, and the model of cardiac hypertrophy was established by aortic banding\u2010induced pressure overload. The results indicate that S100a8\/9 expression was increased in response to pressure overload. S100a9 deficiency alleviated pressure overload\u2010induced hypertrophic response, whereas S100a9 overexpression accelerated cardiac hypertrophy. S100a9\u2010overexpressed mice showed increased FGF23 (fibroblast growth factor 23) expression in the hearts after exposure to pressure overload, which activated calcineurin\/NFAT (nuclear factor of activated T cells) signaling in cardiac myocytes and thus promoted hypertrophic response. A specific antibody that blocks FGFR4 (FGF\u00a0receptor 4) largely abolished the prohypertrophic response of S100a9 in mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">In conclusion, S100a8\/9 promoted the development of cardiac hypertrophy in mice. Targeting S100a8\/9 may be a promising therapeutic approach to treat cardiac hypertrophy.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.122.028006","type":"journal-article","created":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T10:34:13Z","timestamp":1715337253000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":14,"title":["S100a8\/9 (S100 Calcium Binding Protein a8\/9) Promotes Cardiac Hypertrophy Via Upregulation of FGF23 (Fibroblast Growth Factor 23) in Mice"],"prefix":"10.1161","volume":"13","author":[{"given":"Yu\u2010Pei","family":"Yuan","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhuo\u2010Yu","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9481-8185","authenticated-orcid":false,"given":"Teng","family":"Teng","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Si\u2010Chi","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun\u2010Yan","family":"Kong","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao\u2010Feng","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan China"},{"name":"Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5529-6000","authenticated-orcid":false,"given":"Marion","family":"A. 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