ITGA5 and ovarian carcinoma: It has been found that ITGα5/β1 promoted the production of nitric oxide to inhibit the apoptosis of rBMSCs and promote the differentiation of HPASMC.[32] Moreover, ITGα5/β1 has been regarded to promote mesothelial cell proliferation and peritoneal metastasis of ovarian cancer cells.[33] Our results suggested that SPP1‐ITGα5/β1 is an intracellular signal transduction pathway, in which SPP1 in degenerative NPs mediated intracellular mitochondrial dysfunction and inhibits mitophagy by activating ITGα5/β1, accelerating cellular aging, which in turn affects extracellular matrix homeostasis.