ReviewFrontiers in cardiovascular medicine2026
Therapy-induced senescence in breast cancer and cardiovascular disease: a double-edged biological process.
Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Therapy-induced senescence (TIS) has emerged as a central biological response to anticancer therapies, extending beyond tumor suppression to influence long-term tissue homeostasis, cardiovascular (CV) remodeling, and accelerated biological aging. In breast cancer (BC), chemotherapy, radiotherapy, targeted therapies, and emerging immune-activating treatments can induce senescence not only in malignant cells, where it may initially contribute to tumor growth arrest and immune-mediated clearance, but also in non-malignant CV tissues. Persistent accumulation of senescent cells and sustained release of the senescence-associated secretory phenotype (SASP) represent a double-edged sword that may promote chronic inflammation and endothelial dysfunction while contributing to the exacerbation of multifactorial CV outcomes, including myocardial fibrosis, vascular stiffness, and progressive CV dysfunction. Importantly, these outcomes cannot be attributed to TIS alone, as direct therapy-related injury and pre-existing CV risk factors may also contribute. Increasing evidence suggests that TIS-associated mechanisms - including persistent DNA damage response activation, p53/p21- and p16^INK4a^-mediated cell-cycle arrest, NF-
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