<b>Conclusion:</b> This study demonstrates that CXCR4 pathway contributes to pathogenesis of cardiac fibrosis in dilated cardiomyopathy, and it represents a new potential therapeutic target in heart failure.
TGF-beta1 is involved in pathologic states such as cardiac hypertrophy and cardiac fibrosis; we thus postulate that the TGF-beta1 polymorphism is related to LVH in hypertensives.
ELTD1 deficiency exacerbates cardiac hypertrophy and cardiac function induced by AB-induced pressure overload by promoting both cardiomyocyte hypertrophy and cardiac fibrosis.
Galectin-3, a β-galactoside binding lectin, has been described as a mediator of cardiac fibrosis in experimental studies and as a risk factor associated with cardiovascular events in subjects with heart failure.
DDR2 is a tyrosine kinase collagen receptor and is associated with pathological scarring of multiple organs; nevertheless, the functional role of DDR2 in the myocardium remains unclear.George et al. present evidence for the first time that Ang II induces cardiac fibrosis by enhancing DDR2 expression in cardiac fibroblasts via p38 mitogen activated protein kinase (p38 MAPK)-mediated activation of nuclear factor-κB (NF-κB).
Urotensin II (U-II/UTS2) induces cardiac fibrosis by increasing fibroblast collagen synthesis and increased U-II plasma levels have been reported in patients with atrial fibrosis.
AGGF1 inhibits VE-cadherin phosphorylation, increases plasma membrane VE-cadherin in ECs and in mice, blocks vascular permeability induced by ischaemia-reperfusion (IR), restores depressed cardiac function and contraction, reduces infarct sizes, cardiac fibrosis and necrosis, haemorrhages, edema, and macrophage density associated with IR.
Fibroblast growth factor 23 (FGF23) has been reported to induce left ventricular hypertrophy, but it remains unclear whether FGF23 plays a role in cardiac fibrosis.
FAK has recently received attention as a potential mediator of fibrosis, our previous study reported that pharmacological inhibition of FAK can attenuate cardiac fibrosis in post MI models.