Reviewing the Regulation of Autophagy in Aging

Autophagy, a collection of processes by which a cell breaks down damaged components to recycle their materials, is important in many mechanisms known to extend life in various laboratory animals. Better maintained cells are better for a longer life: more autophagy is a good thing, but it declines with age, because of a gradual buildup of materials that cannot be recycled and thus clog up the cellular components that perform autophagy - and for other, less well understood reasons. Here is an open access review on some of the controlling mechanisms: "One part of the aging process involves a decline in cellular housekeeping functions disturbing the maintenance of organism homeostasis. The accumulation of damaged and defective components increases cellular stress, for example, oxidative stress, which activates cellular defence mechanisms including NF-κB signaling pathway and innate immunity system, such as inflammasomes. Aging is associated with a low-grade proinflammatory phenotype which further interferes with housekeeping and cellular homeostasis. Recent studies have indicated that autophagy is a crucial cleansing system preventing inflammation but its capacity clearly declines with aging. The NF-κB signaling system and the autophagic degradation pathway have been closely conserved during evolution and emerging studies indicate that these systems have many context-dependent interactions with each other. We will review the recent literature on the control mechanisms of autophagy by NF-κB signaling and particularly we will focus on its context-dependent regulation during the aging process."



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