Altogether the above results proved and provided evidence for Col11a1 deficiency in DDH development and joint degeneration in vitro and in vivo from the perspective of scRNA‐seq profiles, which demonstrated that the Col11a1 deficiency could impact chondrocyte homeostatic state by dysregulated TCA cycle with increased OXPHOS, alter the chondrocyte cluster frequency by decreased GAG biosynthesis, and impacting cell cycle with higher ferroptosis and cellular senescence to aggravate joint degeneration. The gene discussed is COL11A1; the disease is Hip dysplasia.