NCT06313645Recruiting
Vascular Senescence and Atherosclerotic Plaque Vulnerability
Cellular and Molecular Mechanisms of Vascular Senescence and atherosclerotIC Plaque Vulnerability: the TelOmere-mitochondRIa Cross-tAlk Study
Source: ClinicalTrials.gov · Last updated 16 Apr 2026
Brief summary (registry, in English)
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.
- Status (registry)
- Recruiting
- Study type
- Observational
- Enrollment
- 300 (estimated)
- First submitted
- 11 Mar 2024
- Start date
- 1 Jul 2023
- Primary completion date
- 1 Jul 2026
- Lead sponsor
- Niguarda Hospital
- Diseases
- Coronary artery disease
- NCT number
- NCT06313645
What you commit to
- Study type: Observational
- Planned participants: 300
- From 1 Jul 2023 to the primary completion date, 1 Jul 2026
- 1 site in 1 country
- Visits and tests: ask the trial team, the registry does not list them
Built from the registry fields of ClinicalTrials.gov. It describes the study, not your situation.
Who cannot take part
Copied verbatim from ClinicalTrials.gov and grouped by topic. Only the trial team decides who can take part.
Other illness
- cardiac shock
- congestive heart failure
- end stage renal diseases
- active cancer
Other
- coronary artery bypass graft
Who the study is looking for
- Patients with acute coronary syndromes (unstable angina, non-ST segment elevation myocardial infarction (NSTEMI), ST segment elevation myocardial infarction (STEMI))
- stable angina
- non-angiographically significant coronary diseases recovered for elective diagnostic or interventional procedures
Age in the registry: 18 years to 75 years · Sex: All · Does not accept healthy volunteers
Sites (1)
Sites in registry order. Pick your city on the disease page to sort them by distance.
| Site | City | Country | Site status |
|---|---|---|---|
| ASST GOM Niguarda Coordinator of this site? Confirm its status | Milan | Italy | Recruiting |
This page is information, not medical advice. Discuss any trial with your doctor.