Vascular Senescence and Atherosclerotic Plaque Vulnerability - Trial NCT06313645

Timeline & Enrollment

Primary Outcome

Telomere length

Summary

Chronological aging significantly contributes to structural and functional alterations in the
 vasculature, making it a major risk factor for atherosclerotic disease and its acute
 thrombotic events. DNA damage, including telomeric, non-telomeric, and mitochondrial damage,
 is recognized as a key initiator of vascular aging and atherogenesis. There is abundant
 evidence indicating the presence of oxidative DNA lesions, telomere erosion, and
 mitochondrial DNA damage in both experimental and human plaques, as well as in the peripheral
 cells of atherosclerotic patients.
 
 It is increasingly evident that genomic instability activates signaling pathways that lead to
 a multitude of pathophysiological cellular and molecular changes. These changes promote
 inflammation, apoptosis, autophagy, and ultimately, cellular senescence, accompanied by the
 senescence-associated secretory phenotype (SASP). However, the precise mechanisms linking
 the DNA damage response (DDR) to senescence, SASP in vascular cells, and the pathogenesis of
 atherosclerosis and vulnerable atheroma are yet to be fully understood. Additional research
 is needed to delineate the underlying mechanisms through which mitochondrial dysfunction
 influences telomere length and vice versa, and how their interaction contributes to the
 vascular aging process. Progress in this area has the potential to uncover therapeutic
 targets and novel, more precise diagnostic, and prognostic indicators.
 
 The objectives of the VICTORIA study are to examine the levels of aging-related non-coding
 RNA deregulation (specifically lncRNA TERRA and mitomiR) and peripheral markers of cell aging
 (including telomere length and mitochondrial DNA content) across the various spectra of
 angina pectoris (stable angina, unstable angina, NSTEMI, and STEMI). Additionally, the study
 aims to determine whether these markers are correlated with vulnerable plaque characteristics
 and major adverse cardiovascular events.

ICD-10 Classifications