成纤维细胞生长因子（FGF）23与FGF受体4诱导的心脏线粒体功能障碍作为慢性肾脏病的新靶点？
Fibroblast growth factor (FGF) 23 and FGF receptor 4 induced cardiac mitochondrial dysfunction as a new target in CKD?
作者信息
Haffner Dieter, Leifheit-Nestler Maren
机构信息
Department of Pediatric Kidney, Liver, Metabolic and Neurological Diseases, Hannover Medical School, Hannover, Germany.
Department of Pediatric Kidney, Liver, Metabolic and Neurological Diseases, Hannover Medical School, Hannover, Germany.
出版信息
Kidney Int. 2025 May;107(5):782-784. doi: 10.1016/j.kint.2025.02.017.
Chronic kidney disease is associated with excessive cardiovascular mortality, which is promoted by the phosphaturic hormone fibroblast growth factor 23 (FGF23). Increased FGF23 levels result in left ventricular hypertrophy via activation of the FGF receptor 4 activation. Fuchs et al. now demonstrate, using bioengineered cardiobundles, neonatal rat ventricular myocytes, and mice with chronic kidney disease, that FGF23-FGF receptor 4 activation is a potential mechanism of cardiac mitochondrial dysfunction and metabolic remodeling as early complications of chronic kidney disease, preceding structural cardiac changes.
慢性肾脏病与心血管疾病死亡率过高相关，而排磷激素成纤维细胞生长因子23（FGF23）会加剧这种情况。FGF23水平升高通过激活FGF受体4导致左心室肥厚。富克斯等人现在利用生物工程心脏束、新生大鼠心室肌细胞以及患有慢性肾脏病的小鼠证明，FGF23-FGF受体4激活是慢性肾脏病早期并发症中心脏线粒体功能障碍和代谢重塑的潜在机制，早于心脏结构改变。
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