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Cellular Senescence in Cardiovascular and Metabolic Diseases


Today, we wanted to bring your attention to a new open access paper. The authors here review the role of cellular senescence in the context of the cardiovascular and metabolic diseases of aging. This paper puts special focus on the aging of the vascular system and the role that accumulating numbers of senescent cells play in that process.

What is cellular senescence?

As the body ages, increasing amounts of cells enter a state of senescence. Senescent cells do not divide or support the tissues of which they are a part; instead, they emit a range of potentially harmful signals known collectively as the senescence-associated secretory phenotype (SASP). Senescent cells normally destroy themselves via a programmed process called apoptosis, and they are removed by the immune system; however, as the immune system weakens with age, increasing numbers of these senescent cells escape this process and build up.

By the time people reach old age, significant numbers of these senescent cells have accumulated in the body and cause havoc; they drive the aging process further, they increase the risk of diseases, and the SASP causes other nearby cells to become senescent, thus increasing the scale of the problem further.

This ability of senescent cells to infect neighboring cells is sometimes called the ‘bystander effect’ and is also part of altered intercellular communication, another process of aging. Senescent cell accumulation causes many problems: it degrades tissue function, increases chronic inflammation that drives the aging process [2], and can even eventually raise the risk of cancer [3] and heart disease [4-5] while shortening lifespan [6].

The removal of these cells is therefore a potential avenue of therapy [7-8]. Indeed, senescent cells’ eradication has been the focus of numerous recent research efforts that have shown some spectacular results [9-11].


In aging societies, the discrepancy between the total lifespan and the healthy lifespan is becoming a major problem. Chronological aging is associated with a higher prevalence of age-related diseases, including heart failure, diabetes, and atherosclerotic disorders with or without various comorbidities, resulting in impairment of the quality of life by the limitation of normal activities. Thus, aging is associated with several undesirable processes. The mechanisms of aging and age-associated disorders are complex, and thus cannot be comprehended by a simple approach. However, recent studies have indicated a pivotal role of cellular senescence in the progression of age-related disorders. Back in the 1960s, Hayflick et al. demonstrated that fibroblasts have limited potential to replicate, indicating that aging also occurs at the cellular level. Such aging of cells is currently described as “cellular senescence”. Senescent cells become enlarged and flattened. In association with proliferative arrest, alterations of gene expression by these cells lead to secretion of pro-inflammatory molecules. This is known as the senescence-associated secretory phenotype, and it results in chronic sterile inflammation that promotes tissue remodeling. Senescent cells have been found in various organs of animal models, as well as in elderly humans and persons with age-related disorders. There is evidence that cellular senescence in the vasculature, termed “vascular senescence”, is crucially involved in the pathogenesis of cardiovascular and metabolic disorders. Vascular senescence has been reported to promote atherosclerosis, systolic cardiac dysfunction, and systemic metabolic dysfunction. In this review, we delineate the role of cellular senescence in the diseases associated with aging, focusing on vascular senescence in cardiovascular and metabolic disorders, and discuss the potential usefulness of therapies targeting senescent cells.


Fortunately, companies such as Unity Biotechnology will shortly be bringing the fruits of this line of research into human clinical trials. If you would like to know more, you can read more about the promise and progress of senescent cell removal.


[1] Katsuumi, G., Shimizu, I., Yoshida, Y., & Minamino, T. (2018). Vascular senescence in cardiovascular and metabolic diseases. Frontiers in Cardiovascular Medicine, 5, 18.

[2] Freund, A., Orjalo, A. V., Desprez, P.-Y., & Campisi, J. (2010). Inflammatory Networks during Cellular Senescence: Causes and Consequences. Trends in Molecular Medicine, 16(5), 238–246

[3] Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010). The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression. Annual Review of Pathology, 5, 99–118

[4] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.

[5] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging cell.

[6] Baker, van Deursen et al (2016) Naturally occurring p16Ink4a-positive cells shorten healthy lifespan nature 16932.

[7] Tchkonia, T., Zhu, Y., Van Deursen, J., Campisi, J., & Kirkland, J. L. (2013). Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. The Journal of clinical investigation, 123(3), 966-972.

[8] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.

[9] Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., Van De Sluis, B., … & van Deursen, J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 479(7372), 232-236.

[10] Zhu, Y., Tchkonia, T., Fuhrmann‐Stroissnigg, H., Dai, H. M., Ling, Y. Y., Stout, M. B., … & Wren, J. D. (2016). Identification of a novel senolytic agent, navitoclax, targeting the Bcl‐2 family of anti‐apoptotic factors. Aging cell, 15(3), 428-435.

[11] Yosef, R., Pilpel, N., Tokarsky-Amiel, R., Biran, A., Ovadya, Y., Cohen, S., … & Ben-Porath, I. (2016). Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL. Nature communications, 7.

About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 600 articles on the topic, interviewed over 100 of the leading researchers in the field, hosted livestream events focused on aging, as well as attending various medical industry conferences. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Swiss Monthly, Keep me Prime, and New Economy Magazine. Steve is one of three recipients of the 2020 H+ Innovator Award and shares this honour with Mirko Ranieri – Google AR and Dinorah Delfin – Immortalists Magazine. The H+ Innovator Award looks into our community and acknowledges ideas and projects that encourage social change, achieve scientific accomplishments, technological advances, philosophical and intellectual visions, author unique narratives, build fascinating artistic ventures, and develop products that bridge gaps and help us to achieve transhumanist goals. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project.
  1. Dennis Fink
    March 28, 2018

    Ray Kurzweil in a 5 Dec 2017 dated You Tube conversation w/ Peter Diamandis said he thinks he has personally succeeded in ending his own aging! Someone needs to ask him for the details and put it on the Web so we can test it to see how many people it works for!

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