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.

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