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Aim   Hypertension is a complicated disorder with multifactorial etiology and high heritability. Our previous work has identified  L3MBTL4  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  L3MBTL4 -induced vascular remodeling and exploring the potential mechanism of  L3MBTL4  in vascular smooth muscle cells (VSMCs).Methods   We evaluated the contribution of  L3MBTL4  on proliferation, migration, and phenotype changes of VSMCs and further explored the critical role of p38 and JNK signaling pathway underlying.Results   In  L3MBTL4  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  L3MBTL4  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  L3MBTL4  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  L3MBTL4  and p38/JNK to counteract the progression of hypertension.

p38/JNK Is Required for the Proliferation and Phenotype Changes of Vascular Smooth Muscle Cells Induced by L3MBTL4 in Essential Hypertension