Sox6 enhances vascular smooth muscle cell phenotypic switching and elevates blood pressure by activating autophagy
Background: Sox6 has been shown to play a crucial role in the development of the cardiovascular system. However, its potential role in hypertension and vascular function remains unclear. Methods:  In vascular smooth muscle cells (VSMCs), we employed gain- and loss-of-function approaches combined with RNA sequencing, autophagy flux assessment, and phenotype characterization. Additionally, we established a mouse model with Sox6 overexpression via adeno-associated virus 2 (AAV2) to validate the findings in vivo. Conclusions: Our findings revealed that Sox6 regulates VSMC plasticity and elevates blood pressure by activating autophagy. Therefore, Sox6 inhibition potentially represents a novel strategy for treating hypertension and vascular remodeling. Overall design: RNA-seq profiling of control and Sox6 knockdown mouse vascular smooth muscle cells (VSMCs).