Pathophysiological roles of FGF signaling in the heart.

Pathophysiological roles of FGF signaling in the heart.
复制标题

DOI:
10.3389/fphys.2013.00247
复制
发表时间:
2013-09-06
影响因子:
4
通讯作者:
Ohta H
Ohta H
中科院分区:
医学2区
文献类型:
--
作者:
Itoh N;Ohta H

文献摘要

参考文献

被引文献

相似文献

心脏重塑发展为心力衰竭,这是发病率和死亡率的主要原因。心肌因子,心脏分泌的蛋白质,可能在心脏重塑中发挥作用。成纤维细胞生长因子(FGFs)是一种具有多种功能的分泌蛋白,主要在发育和代谢过程中发挥作用。然而,一些FGFs作为心肌因子在心脏重塑中发挥病理生理作用。FGF2通过激活FGF受体(FGFR) 1c激活MAPK信号,促进心脏肥大和纤维化。相反,FGF16可能通过与FGF2竞争FGFR1c的结合位点来阻止这些。FGF21通过激活FGFR1c和β-Klotho作为共受体来激活MAPK信号,从而防止心脏肥厚。相反,FGF23通过激活钙调神经磷酸酶/NFAT信号而不激活α - klotho诱导心肌肥厚。这些FGFs通过不同的作用机制在心脏重塑中发挥关键作用。这些发现为FGFs在心脏中的病理生理作用提供了新的见解,并可能为心力衰竭提供潜在的治疗策略。
Cardiac remodeling progresses to heart failure, which represents a major cause of morbidity and mortality. Cardiomyokines, cardiac secreted proteins, may play roles in cardiac remodeling. Fibroblast growth factors (FGFs) are secreted proteins with diverse functions, mainly in development and metabolism. However, some FGFs play pathophysiological roles in cardiac remodeling as cardiomyokines. FGF2 promotes cardiac hypertrophy and fibrosis by activating MAPK signaling through the activation of FGF receptor (FGFR) 1c. In contrast, FGF16 may prevent these by competing with FGF2 for the binding site of FGFR1c. FGF21 prevents cardiac hypertrophy by activating MAPK signaling through the activation of FGFR1c with β-Klotho as a co-receptor. In contrast, FGF23 induces cardiac hypertrophy by activating calcineurin/NFAT signaling without αKlotho. These FGFs play crucial roles in cardiac remodeling via distinct action mechanisms. These findings provide new insights into the pathophysiological roles of FGFs in the heart and may provide potential therapeutic strategies for heart failure.
DOI: 10.1111/gtc.12055
发表时间: 2013-07
期刊: Genes to cells : devoted to molecular & cellular mechanisms
影响因子: --
作者:
Matsumoto E;Sasaki S;Kinoshita H;Kito T;Ohta H;Konishi M;Kuwahara K;Nakao K;Itoh N
通讯作者: Itoh N
DOI: 10.1038/nrm3528
发表时间: 2013-03
期刊: Nature reviews. Molecular cell biology
影响因子: --
作者:
通讯作者: --
DOI: 10.1016/j.molmed.2010.12.003
发表时间: 2011-04
影响因子: 13.6
作者:
Doroudgar S;Glembotski CC
通讯作者: Glembotski CC
DOI: 10.1002/jcp.21357
发表时间: 2008-04-01
影响因子: 5.6
作者:
Kharitonenkov, Alexei;Dunbar, James D.;Shanafelt, Armen B.
通讯作者: Shanafelt, Armen B.
DOI: 10.1172/jci61405
发表时间: 2012-07-01
影响因子: 15.9
作者:
Shalhoub, Victoria;Shatzen, Edward M.;Richards, William G.
通讯作者: Richards, William G.