Accumulating evidence points to genotoxic stress as the central cause of aging, leading to most, if not all, other aging hallmarks. Thus, genomic instability could represent an unifying therapeutic target against aging co-morbidities. Using multi-methodological approaches to study cellular and mouse models of aging and progeroid syndromes, our group has validated in recent years the senotherapeutic impact of unprecedented strategies targeting genomic instability. Our most recent findings will be presented.

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