ORIGINAL ARTICLE
Year : 2023 | Volume
: 66 | Issue : 5 | Page : 306--312
Paricalcitol improved cardiac hypertrophy and fibrosis through upregulation of fibroblast growth factor-23 and downregulation of transforming growth factor-beta in a rat model of isoproterenol-induced cardiomyopathy
Chieh-Jen Wu1, Yu-He Li2, Hsin-Hung Chen3
1 Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
2 Department of Laboratory Medicine, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan
3 Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Correspondence Address:
Dr. Hsin-Hung Chen
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, No. 386, Dazhong 1st Road, Zuoying Dist., Kaohsiung 813414
Taiwan
Acute cardiomyopathy is a significant global health concern and one of the leading causes of death in developed countries. Prior studies have shown an association between acute cardiomyopathy and low vitamin D levels. Although paricalcitol, a vitamin D receptor (VDR) activator, has demonstrated clinical benefits in patients with advanced kidney disease, its effect on cardiac remodeling in cardiomyopathy is unknown. This study aimed to investigate the relative effects of paricalcitol on cardiomyopathy in rats. Wistar–Kyoto rats were administered vehicle (sham control group) or isoproterenol to induce cardiomyopathy. Rats administered isoproterenol were subsequently treated with paricalcitol (experimental group) or vehicle (isoproterenol group). Picrosirius red and immunofluorescence staining were used to analyze cardiac fibrosis and hypertrophy. Immunohistochemistry staining was used to confirm the molecular mechanisms involved in isoproterenol-induced cardiomyopathy in rats. Injection of paricalcitol could reduce collagen and transforming growth factor-beta 1 (TGF-β1) levels while activating fibroblast growth factor receptor 1 (FGFR1) and fibroblast growth factor-23 (FGF23) without the help of Klotho, thereby reducing myocardial hypertrophy and fibrosis. As a VDR activator, paricalcitol reduces isoproterenol-induced cardiac fibrosis and hypertrophy by reducing the expression of TGF-β1 and enhancing the expression of VDR, FGFR1, and FGF23.
How to cite this article:
Wu CJ, Li YH, Chen HH. Paricalcitol improved cardiac hypertrophy and fibrosis through upregulation of fibroblast growth factor-23 and downregulation of transforming growth factor-beta in a rat model of isoproterenol-induced cardiomyopathy.Chin J Physiol 2023;66:306-312
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How to cite this URL:
Wu CJ, Li YH, Chen HH. Paricalcitol improved cardiac hypertrophy and fibrosis through upregulation of fibroblast growth factor-23 and downregulation of transforming growth factor-beta in a rat model of isoproterenol-induced cardiomyopathy. Chin J Physiol [serial online] 2023 [cited 2023 Dec 4 ];66:306-312
Available from: https://www.cjphysiology.org/article.asp?issn=0304-4920;year=2023;volume=66;issue=5;spage=306;epage=312;aulast=Wu;type=0 |
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