{"type":"trials","record":{"id":27998,"source_id":"clinicaltrials-gov","external_id":"NCT03928769","title":"PROGENitors, TELomeres and ARTerial Aging","brief_summary":"The prevailing view in telomere epidemiology is that leukocyte telomere length (LTL) is associated with atherosclerotic cardiovascular disease (ACVD) since it serves as a biomarker of the cumulative burden of inflammation and oxidative stress during adult life. However, our recent results indicate that telomere length (TL) is mainly determined before adulthood, by TL at birth and TL attrition during growth. They also demonstrate that short telomeres precede the clinical manifestation of atherosclerosis. The investigators therefore hypothesize that LT is not a simple marker, but a major determinant of arterial aging. Two mechanistic hypotheses may explain an active role of short telomeres in accelerated arterial aging and development of ACVD. The first is that a short TL at the leukocyte level reflects a short TL in endothelial progenitor cells (EPC). Cell replicative capacity being TL-dependent, short telomeres in the EPC would therefore be responsible for diminished replication capacity and vascular repair potential, thereby increasing the vulnerability for developing age-related arterial diseases. The second hypothesis is that a short LTL reflects short TL in arterial wall cells, leading to an increase in the number of senescent vascular cells. Senescent cells are known to alter their secretion pattern, a phenomenon called senescence-associated secretory phenotype (SASP), and thus contribute to tissue injury by promoting inflammation and tissue remodeling leading to lesion progression. These assumptions cannot be tested by LTL measurements alone. The investigators propose, therefore, a model that makes it possible to examine different elements of TL dynamics in different tissues and cell types: leukocytes, circulating EPCs, in situ EPCs and arterial resident cells (mainly smooth muscle cells) in patients with or without atherosclerosis. Our model is based on the following observations: * TL is synchronized (equivalent) across somatic tissues/cells of the newborn: an individual with short telomeres (relative to his pairs) in one tissue should also have short telomeres (relative to his pairs) in other tissues. * TL in EPCs (both circulating and in situ) determines the cell proliferative ability and therefore capacity for vessels repair during aging. * TL in the cells of the arterial wall determines the number of senescent cells that therefore contribute to tissue injury through their change of phenotype. The general aim of the present project is to examine the mechanistic links between arterial aging and TL in these different cell types.","overall_status":"Suspended","phases":[],"study_type":"OBSERVATIONAL","sponsor":"Central Hospital, Nancy, France","enrollment":100,"countries":["France"],"start_date":"2019-05-08","completion_date":"2021-10-20","last_update_date":"2021-04-15","source_url":"https://clinicaltrials.gov/study/NCT03928769","editorial_summary":"A registered study indexed because it matched monitored longevity research terms. Registry status: Suspended. Registration does not establish safety or effectiveness.","first_seen_at":"2026-09-25T00:17:08.561263+00:00","last_seen_at":"2026-09-25T06:20:04.694+00:00","metadata":{"sex":"ALL","acronym":"PROGENTELART","age_range":"18 Years","comparator":null,"organization":"Central Hospital, Nancy, France","interventions":[],"registry_source":"ClinicalTrials.gov","outcome_measures":["Circulating EPC levels — Inclusion visit","Tissue EPC levels — Inclusion visit","TL in EPC — Inclusion visit"],"design_description":null,"source_has_results":false},"controlled_terms":["Atherosclerosis of Artery"],"relevance_confidence":100,"source_quality_score":100,"freshness_score":50,"publication_state":"published","match_explanation":"Title contains controlled term: telomere.","quality_checked_at":"2026-09-25T06:20:05.499352+00:00","duplicate_cluster_key":"id:nct03928769","duplicate_of_id":null,"evidence_snapshot":{"status":"structured","version":1,"duration":"2019-05-08 to 2021-10-20","comparator":null,"confidence":"structured-source","population":"ALL · 18 Years","provenance":{"duration":"start_date and completion_date","comparator":"registry arm fields","population":"registry eligibility fields","intervention":"registry intervention fields","participants":"enrollment","study_design":"study_type and registry design fields","evidence_stage":"phases","reported_outcome":"not available","outcomes_measured":"registry outcome-measure fields"},"generated_at":"2026-09-25T06:20:04.706Z","intervention":[],"participants":100,"study_design":"OBSERVATIONAL","subject_scope":"Human clinical study registration","evidence_stage":"Phase not reported","safety_context":"Eligibility, adverse-event details, and clinical decisions must be checked in the official registry and with qualified clinicians.","source_support":"Structured registry protocol metadata; no finding-level conclusion is generated.","main_limitation":"This is a study registration. No reusable structured result is available here, so it cannot show whether the intervention worked or was safe.","reported_outcome":null,"outcomes_measured":["Circulating EPC levels — Inclusion visit","Tissue EPC levels — Inclusion visit","TL in EPC — Inclusion visit"],"regulatory_context":"Trial registration is not regulatory approval and does not establish that an intervention is available."},"clinical_trial_topics":[{"topic_slug":"telomeres-telomerase","is_published":true,"match_reasons":["Title contains controlled term: telomere.","Abstract contains controlled term: telomere.","Title supplies longevity context: aging.","Study type is explicitly identified as OBSERVATIONAL."],"matched_fields":["title","abstract","title context","study type"],"relevance_score":100,"intelligence_topics":{"name":"Telomeres and telomerase","slug":"telomeres-telomerase"}}],"content_sources":{"name":"ClinicalTrials.gov","homepage_url":"https://clinicaltrials.gov/"}},"canonical_url":"https://www.immortal.life/trials/27998","automation_disclosure":"Generated automatically from cited source metadata. No scientist, clinician, researcher, editor, or human reviewer evaluates this publication before release."}