BI1 was downregulated in response to the IR injury in the infarcted area. WT mice underwent the 45-min ischemia and 0–24-h reperfusion (IR injury, n = 6/group). Subsequently, hearts were obtained and infarcted tissues were isolated. Then, these tissues were used to perform the western blots, immunohistochemistry assay and electron microscope analysis. a The transcription of BI1 in reperfused hearts. b, c The expression of BI1 was detected via western blots. d, e The CMECs were isolated from WT mice and underwent the HR injury. BI1 expression was detected via western blots. f, g Immunohistochemistry of BI1 in WT and BI1TG mice under IR injury and at least 15 microvascular lumens in at least 5 randomly selected fields were observed per group. The boxed area (microvascular lumens) under each micrograph represents the amplification of the black square. h–j The cardiac damage markers were measured via ELISA. k–m The cardiac function in reperfused hearts was evaluated. n Gelatin-ink vascular imaging was used to detect the microvascular perfusion defect. o The HE staining of erythrocyte aggregation secondary to the vasodilation imbalance. BI1 alleviated the erythrocyte accumulation. p The change in the microvascular ultrastructure by EM in response to IR. IR injury induced microvascular wall destruction and luminal stenosis. These changes were reversed by the reintroduction of BI1. q, r TUNEL assay for the apoptotic endothelial cells and at least 15 microvascular lumens in at least 5 randomly selected fields were observed per group. s, t Cardiac microvascular endothelial cells (CMECs) were isolated from WT and BI1TG mice. And then, CMEC underwent 45-min hypoxia and 6-h reoxygenation in vitro. Cellular viability was detected via MTT assay and caspase-3 activity.#P < 0.05 versus the sham group or control group; *P < 0.05 versus IR + WT group or HR + WT cell group