Atrial fibrillation (AF) is an ageing-related chronic disease.
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Atrial electrical and structural remodeling act as substrate for AF maintenance.
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Atrial fibrosis is regarded as basis for atrial fibrillation development and maintenance.
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Senescence contributes to AF by causing atrial fibrosis through extracellular matrix, Angiotensin II, TGF-ß/Smad and thrombin signalling.
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Eliminating senescent cardiac cells by means of senolytic compounds, immune cells, CAR T cells and sEVs may attenuate atrial fibrillation.
Abstract
Cellular senescence is a state of growth arrest that occurs after cells encounter various stresses. Senescence contributes to tumour suppression, embryonic development, and wound healing. It impacts on the pathology of various diseases by secreting inflammatory chemokines, immune modulators and other bioactive factors. These secretory biosignatures ultimately cause inflammation, tissue fibrosis, immunosenescence and many ageing-related diseases such as atrial fibrillation (AF). Because the molecular mechanisms underpinning AF development remain unclear, current treatments are suboptimal and have serious side effects. In this review, we summarize recent results describing the role of senescence in AF. We propose that senescence factors induce AF and have a causative role. Hence, targeting senescence and its secretory phenotype may attenuate AF.