Key result
Cardiac beta3-adrenergic receptors protect against myocardial fibrosis in response to haemodynamic stress by modulating nitric oxide and oxidant stress-dependent paracrine signaling to fibroblasts.
Why the study?
Does cardiac myocyte-specific expression of beta3AR prevent myocardial fibrosis in mice submitted to transaortic constriction?
Does cardiac myocyte-specific expression of beta3AR prevent myocardial fibrosis in mice submitted to transaortic constriction?
Cardiac beta3AR protect from fibrosis in response to haemodynamic stress by modulating nitric oxide and oxidant stress-dependent paracrine signaling to fibroblasts, suggesting beta3AR agonism as a potential anti-fibrotic therapy.
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β3AR modulation may limit fibrosis via NO; leaves open clinical translation in human heart disease.
Hermida et al. (2017) studied Myocardial fibrosis. Cardiac myocyte beta3-adrenergic receptor (beta3AR) expression vs. beta3AR deletion (c-Adrb3-ko) was evaluated on Myocardial fibrosis and collagen content. Cardiac beta3-adrenergic receptors protect against myocardial fibrosis in response to haemodynamic stress by modulating nitric oxide and oxidant stress-dependent paracrine signaling to fibroblasts.
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