PLXNB1 and diabetes mellitus: Additionally, compared with diabetes mellitus-exosomes, normal-BMSC-exos, highly expressed miR-140–3p, accelerated the repairment process of diabetic wounds by facilitating the osteogenic differentiation of BMSCs through the suppression of plexin B1 which serves as the Sema4D receptor and is involved in the plexin B1/RhoA/ROCK pathways [157].