Daily administration of recombinant human neuregulin-1 prevented cardiac and renal hypertrophy and fibrosis caused by angiotensin II infusion and endothelial nitric oxide synthase deficiency in mice.
NRG1 acts as a compensatory mechanism for eNOS deficiency, and its administration prevents cardiac and renal hypertrophy and fibrosis.
ECs compensate for eNOS deficiency by increasing the secretion of NRG1. NRG1 administration prevents cardiac and renal hypertrophy and fibrosis caused by ANG II infusion and eNOS deficiency. NRG1 expression is regulated by miR-134.
Shakeri et al. (Fri,) conducted a other in Endothelial nitric oxide synthase (eNOS) deficiency (n=84). Recombinant human neuregulin-1 (rhNRG1) vs. Vehicle (PBS) was evaluated on Cardiac and renal hypertrophy and fibrosis. Daily administration of recombinant human neuregulin-1 prevented cardiac and renal hypertrophy and fibrosis caused by angiotensin II infusion and endothelial nitric oxide synthase deficiency in mice.