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Published on: May 31, 2016
Inflammation and Vascular Ageing: From Telomeres to Novel Emerging Mechanisms
Martina Chiriacò1, Georgios Georgiopoulos2, Emiliano Duranti1
1Department of Clinical and Experimental Medicine, Università di Pisa, Santa Chiara Hospital, Via Roma, 67, 56126, Pisa, Italy.
Insights
Inflammation and biological ageing contribute significantly to unexplained cardiovascular disease (CVD) risk. This review explores how cellular ageing drives vascular inflammation, promoting atherosclerosis independently of traditional risk factors.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Gerontology
Background:
- Cardiovascular disease (CVD) is a leading global cause of death.
- Effective treatments targeting known risk factors have reduced CVD burden.
- Residual cardiovascular risk persists despite optimal management of traditional factors.
Purpose of the Study:
- To review evidence linking biological ageing to CVD.
- To explore the role of inflammation as a mediator between ageing and CVD.
- To understand the potential vicious cycle between cellular ageing and vascular inflammation.
Main Methods:
- Review of recent randomized clinical trials.
- Analysis of Mendelian randomization studies.
- Synthesis of current scientific literature on ageing, inflammation, and atherosclerosis.
Main Results:
- Inflammation is implicated in a significant portion of residual cardiovascular risk.
- Accelerated vascular ageing is a recognized mechanism linking inflammation to CVD.
- Cellular ageing contributes to vascular inflammation, potentially driving atherosclerosis.
Conclusions:
- Biological ageing plays a crucial role in cardiovascular disease development.
- Inflammation acts as a key mediator, connecting ageing processes to increased CVD risk.
- A cycle of cellular ageing and vascular inflammation may promote atherosclerosis progression.
Abstract:
Cardiovascular disease (CVD) remains the leading cause of morbility and mortality worldwide. The identification of common cardiovascular risk factors has led to the development of effective treatments that enabled a significant reduction of the global cardiovascular disease burden. However, a significant proportion of cardiovascular risk remains unexplained by these risk factors leaving many individuals at risk of cardiovascular events despite good control of the risk factors. Recent randomized clinical trials and Mendelian randomization studies have suggested that inflammation explains a significant proportion of the residual cardiovascular risk in subjects with good control of risk factors. An accelerated process of vascular ageing is increasingly recognized as a potential mechanism by which inflammation might increase the risk of CVD. In turn, cellular ageing represents an important source of inflammation within the vascular wall, potentially creating a vicious cycle that might promote progression of atherosclerosis, independently from the individual cardiovascular risk factor burden. In this review, we summarise current evidence suggesting a role for biological ageing in CVD and how inflammation might act as a key mediator of this association.
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