BibTex format
@article{Ajjan:2026:eurheartj/ehag095,
author = {Ajjan, RA and Huckstepp, RTR and Akbar, N and Bauersachs, J and Lok, JCW and Choppy-Madeleine, J and Christopher, G and Dalakoti, M and Dawson-Plincke, E and Dodds, J and Ellison-Hughes, GM and Emanueli, C and George, CH and Goyal, A and Higginbotham, V and Holzner, L and Kanamarlapudi, V and Madeddu, P and Mauro, C and Lewis-McDougall, F and Murray, AJ and Damien, Genetus RP and Short, E and Sussman, MA and Tavares, AAS and Thompson, S and Wadodkar, M and Calimport, SRG and Bentley, BL},
doi = {eurheartj/ehag095},
journal = {Eur Heart J},
title = {Senescence-related myocardial dysfunction: keeping a young heart.},
url = {http://dx.doi.org/10.1093/eurheartj/ehag095},
year = {2026}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - The heart, a vital organ, works without interruption and constantly adjusts to the ever-changing demands on our body. It adapts to physiological and pathological changes, including exercise and emotional state, as well as metabolic, respiratory, and vascular abnormalities. The pumping action of the heart is determined by the health of the myocardium, which undergoes changes with ageing that are both under-investigated and incompletely understood, potentially impacting our approach to pathological conditions. Here, the alterations in cellular, tissue, and gross physiological function of the heart with age are discussed. At the molecular level, non-coding RNAs influence cellular senescence, and extracellular vesicles induce fibrosis through matrix remodelling. Mitochondrial dysfunction and altered fatty acid oxidation reduce cellular energetics, whilst accumulation of reactive oxygen species and steatosis, as well as telomere shortening coupled with reduced autophagy, limit the myocardium's regenerative capability. Loss of cardiomyocytes, combined with senescence, requires compensatory hypertrophy, inducing myocardial stiffness and altered muscle function. In addition to these direct alterations in myocardial characteristics with ageing, other factors that can affect the myocardium indirectly are addressed, including valve calcification, resulting in regurgitation and/or stenosis; vascular abnormalities, reducing compliance and exacerbating hypertension; fibrosis leading to cardiac arrhythmias; and autonomic dysregulation, reducing cardiac adaptability. Finally, potential modulation of cardiac ageing is discussed whilst also addressing which senescent modifications should be considered as ageing-related physiological changes of the myocardium. A better understanding of myocardial ageing will differentiate physiological changes from early, preventable, and reversible pathological changes, consequently helping to optimize management of individuals with or at risk of myo
AU - Ajjan,RA
AU - Huckstepp,RTR
AU - Akbar,N
AU - Bauersachs,J
AU - Lok,JCW
AU - Choppy-Madeleine,J
AU - Christopher,G
AU - Dalakoti,M
AU - Dawson-Plincke,E
AU - Dodds,J
AU - Ellison-Hughes,GM
AU - Emanueli,C
AU - George,CH
AU - Goyal,A
AU - Higginbotham,V
AU - Holzner,L
AU - Kanamarlapudi,V
AU - Madeddu,P
AU - Mauro,C
AU - Lewis-McDougall,F
AU - Murray,AJ
AU - Damien,Genetus RP
AU - Short,E
AU - Sussman,MA
AU - Tavares,AAS
AU - Thompson,S
AU - Wadodkar,M
AU - Calimport,SRG
AU - Bentley,BL
DO - eurheartj/ehag095
PY - 2026///
TI - Senescence-related myocardial dysfunction: keeping a young heart.
T2 - Eur Heart J
UR - http://dx.doi.org/10.1093/eurheartj/ehag095
UR - https://www.ncbi.nlm.nih.gov/pubmed/41790041
ER -