protocolSection identificationModule nctId: NCT06313645, orgStudyIdInfo id: B83C22004880006, briefTitle: Vascular Senescence and Atherosclerotic Plaque Vulnerability, acronym: VICTORIA, statusModule overallStatus: RECRUITING, startDateStruct date: 2023-07-01, primaryCompletionDateStruct date: 2025-07-01, completionDateStruct date: 2025-12-31, studyFirstPostDateStruct date: 2024-03-15, lastUpdatePostDateStruct date: 2024-03-19, sponsorCollaboratorsModule leadSponsor name: Niguarda Hospital, class: OTHER, collaborators name: Istituto di Fisiologia Clinica CNR, descriptionModule briefSummary: 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., conditionsModule conditions: Coronary Artery Disease, designModule studyType: OBSERVATIONAL, designInfo observationalModel: COHORT, timePerspective: PROSPECTIVE, enrollmentInfo count: 300, type: ESTIMATED, armsInterventionsModule interventions name: Several biomarkers, outcomesModule primaryOutcomes measure: Telomere length, secondaryOutcomes measure: Mitochondrial DNA copy number (mtDNAcn), secondaryOutcomes measure: MitomiR, secondaryOutcomes measure: Long non-coding (lnc) RNA TERRA, secondaryOutcomes measure: pro-oxidant cytokines, eligibilityModule sex: ALL, minimumAge: 18 Years, maximumAge: 75 Years, stdAges: ADULT, stdAges: OLDER_ADULT, contactsLocationsModule locations facility: ASST GOM Niguarda, status: RECRUITING, city: Milano, state: Lombardia, zip: 20162, country: Italy, contacts name: Jonica Campolo, MSc, role: CONTACT, phone: +39026444, phoneExt: 5578, email: jonica.campolo@ospedaleniguarda.it, contacts name: Emanuela Piccaluga, MD, role: CONTACT, phone: +39026444, phoneExt: 2308, email: emanuela.piccaluga@ospedaleniguarda.it, geoPoint lat: 45.46427, lon: 9.18951, hasResults: False