Some RBPs were previously implicated in the pathological mechanisms of cerebrovascular diseases.[20, 21] For instance, a previous study found that HuR could be modulated by cystathionine γ‐lyase‐induced S‐sulfhydration, and correlated with endothelial dysfunction onset.[22] Furthermore, HuR was reported to regulate the production of angiogenesis‐linked proteins under stimulatory conditions.[23] Additionally, HuR could contribute to ischemia, matrix protein accumulation, and angiogenesis in the kidneys.[24] Herein, HuR promoted angiogenesis and alleviated dysfunction in CIRI mice. Here, ELAVL1 is linked to endothelial dysfunction.