Norepinephrine promotes renal artery vascular smooth muscle cell proliferation, migration, and phenotypic switching through ROCK1 activation and alters mitochondrial dynamics.
The norepinephrine-ROCK1 axis mediates vascular remodeling in renal artery smooth muscle cells, identifying it as a potential therapeutic target for hypertensive nephropathy.
Objectives: This study investigated the role of norepinephrine (NE) and ROCK1 in regulating renal artery vascular smooth muscle cells (rVSMCs). Materials and Methods: rVSMCs were treated with NE, and ROCK1 expression was assessed. Cell proliferation, migration, and phenotypic switching were evaluated using EdU incorporation and wound-healing assays. ROCK1 was silenced by siRNA. Mitochondrial membrane potential and morphology were analyzed to determine NE-induced mitochondrial alterations. Results: NE significantly up-regulated ROCK1 expression in rVSMCs. It promoted proliferation, migration, and phenotypic switching, as indicated by increased expression of proliferative and migratory markers, whereas ROCK1 silencing attenuated these effects. NE also reduced mitochondrial membrane potential and induced mitochondrial fission, suggesting an additional mechanism contributing to vascular remodeling. Conclusion: NE promotes rVSMCs proliferation, migration, and phenotypic switching through ROCK1 activation and alters mitochondrial dynamics. These findings identify the NE-ROCK1 axis as a critical mediator of vascular remodeling in hypertensive nephropathy and suggest it may serve as a promising therapeutic target.
Chen et al. (Thu,) conducted a other in Vascular remodeling in hypertensive nephropathy. Norepinephrine (NE) and ROCK1 siRNA was evaluated on Cell proliferation, migration, phenotypic switching, and mitochondrial dynamics. Norepinephrine promotes renal artery vascular smooth muscle cell proliferation, migration, and phenotypic switching through ROCK1 activation and alters mitochondrial dynamics.