Profiling the molecular and physiological effects of senolytic treatment on aged mice identifies immune, fibrotic and metabolic remodeling.
Abstract
Although senolytics such as dasatinib and quercetin (D+Q) show promise in modulating aging, their tissue-specific efficacy and optimal intervention timing remain poorly understood. Given D+Q's potential off-target effects, incomplete senescent cell clearance and associated hematologic side effects, we performed an unbiased multitissue single-cell analysis in aged mice across different aging phenotypes and tissue contexts. Here through integrative transcriptomics, single-cell technologies, histopathology and molecular profiling, we investigated the influence of D+Q treatment on aging-related phenotypes at the tissue and cellular levels. Specifically, D+Q remodeled immunity by enhancing immune cell function and maintaining population stability, alleviated tissue inflammation and improved metabolic profiles. Furthermore, intervention initiated during early aging and prolonged treatment showed a greater tendency to mitigate readouts of aging compared to shorter, late-stage treatment. Our findings reveal that D+Q systematically attenuates several aging hallmarks in a tissue- and cell-type-specific manner, and support the possibility that early-initiated, long-term intervention may amplify efficacy.
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Research summary
Dasatinib and quercetin treatment in aged mice systematically attenuates multiple aging hallmarks by remodeling immunity, reducing fibrosis, and improving metabolism, with early and prolonged intervention showing superior efficacy. This study provides relevant mechanistic insights into how senolytics modulate fundamental aging processes across tissues, supporting the hypothesis that targeting senescent cells can delay aging phenotypes.
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