p38/JNK Is Required for the Proliferation and Phenotype Changes of Vascular Smooth Muscle Cells Induced by in Essential Hypertension.

Aim: Hypertension is a complicated disorder with multifactorial etiology and high heritability. Our previous work has identified as a novel susceptibility gene for the development of essential hypertension, accompanied with activation of p38/JNK. Yet, little evidence has been reported whether p38/JNK contributed directly to -induced vascular remodeling and exploring the potential mechanism of in vascular smooth muscle cells (VSMCs).

Methods: We evaluated the contribution of on proliferation, migration, and phenotype changes of VSMCs and further explored the critical role of p38 and JNK signaling pathway underlying.

Results: In transgenic rats, we found that the elevated blood pressure, increased left ventricular hypertrophy, and thickened vascular media layer were significantly relieved by both p38 and JNK inhibitors. Meanwhile, increased cell proliferation, advanced cell cycle progression, greater migratory capability, and synthetic phenotype were observed in overexpressed VSMCs, which could be blocked by either p38 or JNK inhibitor.

Conclusions: Our findings pinpointed that p38 and JNK were required for the proliferation and phenotype changes of VSMCs induced by in hypertension. These novel findings yield new insights into the genetic and biological basis of hypertension and are fundamental for further studies to explore the intervention strategies targeting and p38/JNK to counteract the progression of hypertension.