A plethora of studies has indicated that ageing is characterized by an altered proteostasis, ROS accumulation and a status of mild/chronic inflammation, in which macroautophagy reduction and abnormal UPR activation play a pivotal role. The dysregulation of these inter-connected processes favors immune dysfunction and predisposes to a variety of several apparently unrelated pathological conditions including cancer and neurodegeneration. Given the progressive ageing of the population, a better understanding of the mechanisms regulating autophagy, UPR and their interplay is needed in order to design new therapeutic strategies able to counteract the effects of ageing and concomitantly restrain the onset/progression of age-related diseases that represent a private and public health problem.

大量研究表明，衰老的特征是改变了蛋白稳态，ROS积累和轻度/慢性炎症状态，其中巨噬细胞的自噬减少和异常的UPR激活起关键作用。这些相互联系的过程的失调促进了免疫功能障碍，并易患多种明显无关的病理状况，包括癌症和神经变性。鉴于人口的逐渐老龄化，需要更好地了解调节自噬，UPR及其相互作用的机制，以便设计出能够抵消衰老影响并同时抑制与年龄有关的疾病的发作/发展的新治疗策略代表私人和公共卫生问题。