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Cardiac remodeling is the main pathophysiological process of cardiac function deterioration in HF patients. Inflammation is a key factor that stimulates cardiomyocyte hypertrophy, fibroblast proliferation, and transformation leading to myocardial remodeling, which severity is significantly related to the prognosis of patients. SAA1 (Serum amyloid A1) is a lipid\u2010binding protein that was an important regulator involved in inflammation, whose biological functions in the heart remain rarely known. In this research, we intended to test the role of SAA1 in SAA1\u2010deficient (SAA1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ), and wild\u2010type mice were exposed to transverse aortic banding surgery to establish the model of cardiac remodeling. Besides, we assessed the functional effects of SAA1 on cardiac hypertrophy and fibrosis. The expression of SAA1 was increased in the mice transverse aortic banding model induced by pressure overload. After 8\u2009weeks of transverse aortic banding, SAA1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice displayed a lower level of cardiac fibrosis than wild\u2010type mice, but did not significantly influence the cardiomyocyte hypertrophy. In addition, there was also no significant difference in cardiac fibrosis severity between wild\u2010type\u2010sham and knockout\u2010sham mice. These findings are the first to reveal SAA1 absence hinders cardiac fibrosis after 8\u2009weeks of transverse aortic banding. Furthermore, SAA1 deficiency had no significant effect on cardiac fibrosis and hypertrophy in the sham group in this study.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201506r","type":"journal-article","created":{"date-parts":[[2023,4,6]],"date-time":"2023-04-06T11:10:25Z","timestamp":1680779425000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["<scp>SAA1<\/scp>\n                    deficiency alleviates cardiac remodeling by inhibiting\n                    <scp>NF\u2010\u03baB<\/scp>\n                    \/p38\/\n                    <scp>JNK<\/scp>\n                    and\n                    <scp>TGF\u03b2<\/scp>\n                    \/Smad pathways"],"prefix":"10.1096","volume":"37","author":[{"given":"Yusha","family":"Xiao","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Surgery Zhongnan Hospital of Wuhan University  430071 Wuhan China"},{"name":"Hubei Provincial Engineering 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