Our current study demonstrates that Cav-1 plays a critical role in oxLDL-induced endothelial stiffening in vitro and in dyslipidemia and age-related endothelial stiffening in vivo indicating that this process is mediated by the CD36/Cav-1 pathway and suggesting a new mechanism for the athero-protective and possibly anti-ageing effects of Cav-1 depletion. The gene discussed is CAV1; the disease is metabolic syndrome.