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Vascular Senescence and Atherosclerotic Plaque Vulnerability

NCT06313645 · Status: RECRUITING · Type: OBSERVATIONAL · Enrollment: 300

Last updated 2026-04-16

No results posted yet for this study

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.

Conditions

Interventions

OTHER

Several biomarkers

Telomere length Mitochondrial DNA copy number (mtDNAcn) MitomiR long non-coding (lnc) RNA TERRA pro-oxidant cytokines \& chemokines

Sponsors & Collaborators

  • Istituto di Fisiologia Clinica CNR

    collaborator OTHER

  • Niguarda Hospital

    lead OTHER

Principal Investigators

  • Maria Grazia Andreassi, PhD · IFC CNR Pisa

Eligibility

Min Age
18 Years
Max Age
75 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2023-07-01
Primary Completion
2026-07-01
Completion
2027-12-31

Countries

  • Italy

Study Locations

More Related Trials

Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06313645 on ClinicalTrials.gov