| Source: |
Ajjan, R A, Huckstepp, R T R, Akbar, N, Bauersachs, J, Lok, J C W, Choppy-Madeleine, J, Christopher, G, Dalakoti, M, Dawson-Plincke, E, Dodds, J, Ellison-Hughes, G M, Emanueli, C, George, C H, Goyal, A, Higginbotham, V, Holzner, L, Kanamarlapudi, V, Madeddu, P, Mauro, C, Lewis-McDougall, F, Murray, A J, Damien Genetus, R P, Short, E, Sussman, M A, Tavares, A A S, Thompson, S, Wadodkar, M, Calimport, S R G & Bentley, B L 2026, 'Senescence-related myocardial dysfunction : keeping a young heart', European Heart Journal. https://doi.org/10.1093/eurheartj/ehag095 |
| Description: |
The ageing heart undergoes progressive and substantial changes. Myocardial cells enter a senescence-associated secretory phenotype (SASP), associated with alterations in extracellular vesicles (EVs) containing microRNAs, creating an inflammatory environment. These molecular changes, combined with mitochondrial dysfunction, induce myocardial cell hypertrophy, multinucleation, and also result in altered responses to autonomic regulation. Alongside the stress of the continuous workload on the heart over a lifetime, there is a reduction in repair mechanisms, which coupled with fibrosis, steatosis, valve stenosis and compromised blood supply, due to atherosclerosis, ultimately lead to organ dysfunction, and myocardial ageing. Created in Biorender. For image description, please refer to the figure legend and surrounding text. |