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- W2034074791 abstract "The molecular mechanisms underlying heart failure (HF) and recovery remain poorly defined. Recent evidence suggests that activin signalling is altered in HF and we hypothesised that follistatins, which are key regulators of activin signalling and which are involved in skeletal muscle regeneration, may be changed in heart failure and contribute to recovery. We examined follistatin (Fst), follistatin-like1 (Fstl1) and follistatin-like3 (Fstl3/FLRG) gene expression by quantitative real-time RT-PCR in myocardial samples obtained from donor organs with good haemodynamic function (n=9), patients with end-stage dilated cardiomyopathy (DCM, n=25), and from DCM patients who showed cardiac reverse remodelling and recovery from heart failure following combined mechanical unloading using left ventricular assist device (LVAD) and pharmacologic therapy (LVAD, n=15). We found a significant increase in both Fstl1 and Fstl3 expression in HF (1.51±0.46 and 2.1±1.0-fold compared to donors, respectively, P<0.005) with levels returning to normal following recovery, whereas Fst levels did not change. Increased Fstl3 levels in HF correlated with skeletal α-actin and BNP, both markers of disease severity, and were unaltered in response to therapy in LVAD patients who failed to recover. In contrast, Fstl1 levels in HF showed a negative correlation with skeletal α-actin and LVAD implant levels correlated with loss of skeletal α-actin during recovery. The data implicate for the first time Fst3, Fst1 and Fst in the mechanisms underlying heart failure and recovery and open possibilities to new therapeutic tools and targets." @default.
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- W2034074791 date "2007-06-01" @default.
- W2034074791 modified "2023-09-26" @default.
- W2034074791 title "Follistatin gene expression is elevated in heart failure and decreases following recovery" @default.
- W2034074791 doi "https://doi.org/10.1016/j.yjmcc.2007.03.479" @default.
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