Novel roles of Nrf3–Trim5 axis in vascular smooth muscle cell dysfunctions and neointimal hyperplasia

We comprehensively demonstrate that Nrf3 is a novel modulator in VSMC dysfunctions and injury-induced NIH. Nrf3 exerts its pathological functions by transcriptional activation of Trim5 gene, which in turn triggers autophagy in VSMCs and injured arteries, promoting arterial remodelling. Inhibiting the Nrf3-Trim5 signal axis ameliorates injury-induced NIH, offering novel therapeutics for treating patients with NIH-related vascular diseases.