Key result
Cellular senescence may contribute to HF pathogenesis and represents a potential therapeutic target.
Why the study?
Heart failure pathogenesis is not fully understood and current treatment options remain imperfect, requiring deeper insight into disease mechanisms and identification of potential therapeutic targets.
Design
Review
Should not yet alter heart failure management; extends evidence linking senescence to pathogenesis and warrants prospective trials.
Heart failure (HF) significantly limits survival and decreases quality of life. The global incidence of HF is rising. The pathogenesis of HF is not yet fully understood, which results in the present treatment options still being imperfect. Therefore, there is a need to deepen the knowledge about HF pathogenesis and identify potential therapeutic targets. Aging increases the risk of developing HF. Recently, cellular senescence, a stable state of cell cycle arrest induced by various stressors or genomic damage, has been recognized to be involved in HF pathogenesis. Senescent cells may be involved in the development of age‐related diseases. However, cellular senescence may occur in correlation with aging or be age‐independent. Its impact is complex, especially since the heart is composed of different cell types, each of which may undergo senescence in diverse ways. Elimination of senescent cells also emerges as a potential treatment option. This article extensively reviews relations between cellular senescence and HF. Moreover, it describes the role of plasma proteins related to cellular senescence as potential biomarkers and prognostic factors in HF. This review also summarizes data concerning therapeutics targeting senescence in the HF context and implicates future research perspectives.
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Krauz et al. (2026) studied this question. Cellular senescence may play a significant role in the pathogenesis of heart failure, with senescent cells being potential therapeutic targets.
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