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. 2018 Jan 2;217(1):65–77. doi: 10.1083/jcb.201708092

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© 2018 McHugh and Gil

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 1. — Senescence as a central hallmark of aging. Telomere damage, epigenetic dysregulation, DNA damage, and mitochondrial dysfunction are primary drivers of damage in aging. Several of these drivers of damage can induce senescence. Senescence can in turn drive the consequential aging hallmarks in response to damage: stem cell exhaustion and chronic inflammation. Other responses to damage, such as proteostatic dysfunction and nutrient signaling disruption, are also integrally linked with the senescence response. Adapted from López-Otín et al. (2013).