Heart Disease and Ageing: The Roles of Senescence, Mitochondria, and Telomerase in Cardiovascular Disease
- PMID: 37120464
- DOI: 10.1007/978-3-031-26576-1_4
Heart Disease and Ageing: The Roles of Senescence, Mitochondria, and Telomerase in Cardiovascular Disease
Abstract
During ageing molecular damage leads to the accumulation of several hallmarks of ageing including mitochondrial dysfunction, cellular senescence, genetic instability and chronic inflammation, which contribute to the development and progression of ageing-associated diseases including cardiovascular disease. Consequently, understanding how these hallmarks of biological ageing interact with the cardiovascular system and each other is fundamental to the pursuit of improving cardiovascular health globally. This review provides an overview of our current understanding of how candidate hallmarks contribute to cardiovascular diseases such as atherosclerosis, coronary artery disease and subsequent myocardial infarction, and age-related heart failure. Further, we consider the evidence that, even in the absence of chronological age, acute cellular stress leading to accelerated biological ageing expedites cardiovascular dysfunction and impacts on cardiovascular health. Finally, we consider the opportunities that modulating hallmarks of ageing offer for the development of novel cardiovascular therapeutics.
Keywords: Ageing; Atherosclerosis; Cardiovascular; Heart failure; Inflammation; Remodelling; Senescence; Senolytic.
© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG.
References
-
- Abbate A, Trankle CR, Buckley LF, Lipinski MJ, Appleton D, Kadariya D, Canada JM, Carbone S, Roberts CS, Abouzaki N, Melchior R, Christopher S, Turlington J, Mueller G, Garnett J, Thomas C, Markley R, Wohlford GF, Puckett L, Chazal HM, Chiabrando JG, Bressi E, Buono MGD, Schatz A, Vo C, Dixon DL, Biondi-Zoccai GG, Kontos MC, Tassell BWV (2020) Interleukin-1 blockade inhibits the acute inflammatory response in patients with ST-Segment–elevation myocardial infarction. J Am Heart Assoc 9(5):e014941. https://doi.org/10.1161/JAHA.119.014941 - DOI
-
- Ahmad T, Sundar IK, Lerner CA, Gerloff J, Tormos AM, Yao H, Rahman I (2015) Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease. FASEB J 29(7):2912–2929. https://doi.org/10.1096/fj.14-268276 - DOI
-
- Ahmed S, JoF P, Birket MJ, Beckmann T, Brings S, Peters H, Birch-Machin MA, von Zglinicki T, Saretzki G (2008) Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress. J Cell Sci 121(7):1046–1053. https://doi.org/10.1242/jcs.019372 - DOI
-
- Ale-Agha N, Jakobs P, Goy C, Zurek M, Rosen J, Dyballa-Rukes N, Metzger S, Greulich J, von Ameln F, Eckermann O, Unfried K, Brack F, Grandoch M, Thielmann M, Kamler M, Gedik N, Kleinbongard P, Heinen A, Heusch G, Gödecke A, Altschmied J, Haendeler J (2021) Mitochondrial telomerase reverse transcriptase protects from myocardial ischemia/reperfusion injury by improving complex I composition and function. Circulation 144(23):1876–1890. https://doi.org/10.1161/circulationaha.120.051923 - DOI
-
- Alpert A, Pickman Y, Leipold M, Rosenberg-Hasson Y, Ji X, Gaujoux R, Rabani H, Starosvetsky E, Kveler K, Schaffert S, Furman D, Caspi O, Rosenschein U, Khatri P, Dekker CL, Maecker HT, Davis MM, Shen-Orr SS (2019) A clinically meaningful metric of immune age derived from high-dimensional longitudinal monitoring. Nat Med 25(3):487–495. https://doi.org/10.1038/s41591-019-0381-y - DOI
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
