摘要：Ageing is characterized by a general decrease in O 2 supply to tissues and a reduction in tissue pO 2 . A diminished vascularization in ageing alters the diffusion of O 2 at the capillary tissue level, and at an advanced stage, this can lead to tissue hypoxia. Molecular O 2 sensors mediate the response to O 2 deprivation through the regulation of protein expression, enzyme activities, and metabolic regulating factors [1]. HIF1¦Á is perhaps the best-studied responsive mechanism. A critical role in vascularization and angiogenesis is played by VEGF, a HIF1¦Á target. This crucial proangiogenic factor is also regulated at the mRNA level by a non-HIF pathway, DEAD-box RNA helicase [2]. Deficient O 2 supply together with a reduced ability to induce HIF1¦Á expression may contribute to the aetiology of ageing. On the other hand, low O 2 levels lead to neovascularization that can contribute to pathological events such as tumour growth and macular oedema. Furthermore, intermittent or continuous cellular hypoxia represents a source for oxygen radical production that is responsible for the inexorable decline of tissue morphology and physiology with age. In ageing, neovascularization appears to be attenuated which might be linked to impaired HIF1¦Á induction. Other compensatory mechanisms might also take place in conditions of O 2 limitation [1].
