Scharf Andrea, Limke Annette, Guehrs Karl-Heinz, von Mikecz Anna
IUF - Leibniz Research Institute for Environmental Medicine GmbH, Duesseldorf 40225, Germany.
Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
iScience. 2022 Aug 28;25(9):105027. doi: 10.1016/j.isci.2022.105027. eCollection 2022 Sep 16.
Delaying aging while prolonging health and lifespan is a major goal in aging research. One promising strategy is to focus on reducing negative interventions such as pollution and their accelerating effect on age-related degeneration and disease. Here, we used the short-lived model organism . to analyze whether two candidate pollutants corrupt general aging pathways. We show that the emergent pollutant silica nanoparticles (NPs) and the classic xenobiotic inorganic mercury reduce lifespan and cause a premature protein aggregation phenotype. Comparative mass spectrometry revealed that increased insolubility of proteins with important functions in proteostasis is a shared phenotype of intrinsic- and pollution-induced aging supporting the hypothesis that proteostasis is a central resilience pathway controlling lifespan and aging. The presented data demonstrate that pollutants corrupt intrinsic aging pathways. Reducing pollution is, therefore, an important step to increasing healthy aging and prolonging life expectancies on a population level in humans and animals.
延缓衰老同时延长健康寿命是衰老研究的一个主要目标。一种有前景的策略是专注于减少负面干预因素，如污染及其对与年龄相关的退化和疾病的加速作用。在此，我们使用了寿命较短的模式生物……来分析两种候选污染物是否破坏一般衰老途径。我们发现新兴污染物二氧化硅纳米颗粒（NPs）和经典外源性无机汞会缩短寿命并导致过早的蛋白质聚集表型。比较质谱分析表明，在蛋白质稳态中具有重要功能的蛋白质的不溶性增加是内在衰老和污染诱导衰老的共同表型，支持了蛋白质稳态是控制寿命和衰老的核心弹性途径这一假说。所呈现的数据表明污染物会破坏内在衰老途径。因此，减少污染是在人类和动物群体层面增加健康衰老和延长预期寿命的重要一步。
