Cardiovascular risk factors and molecular routes underlying endothelial dysfunction: Novel opportunities for primary prevention.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms, biomarkers, and lifestyle interventions with no new empirical data or systematic search.
PubMed 35643340 · doi:10.1016/j.bcp.2022.115108
What was done
The authors reviewed the molecular mechanisms linking traditional cardiovascular risk factors (aging, hypertension, smoking, hyperglycemia, dyslipidemia) and emerging determinants (fetal factors, gut microbiome alteration, clonal hematopoiesis, air pollution, sleep disorders) to endothelial dysfunction. They synthesized evidence on epigenetic regulation of endothelial nitric oxide synthase, reactive oxygen species generation, circulating biomarker candidates, non-invasive vascular testing via flow-mediated dilation, and lifestyle interventions aimed at restoring endothelial health.
What was found
The abstract reports no numerical data, effect sizes, or trial counts. It qualitatively notes that endothelial dysfunction is driven by reduced nitric oxide bioavailability and increased reactive oxygen species. Circulating levels of endothelial microparticles, endoglin, and endocan are increased, while irisin is decreased, in association with impaired flow-mediated dilation in patients with cardiovascular risk factors. Lifestyle modifications, including smoking cessation, exercise, diet control, and weight loss, can reverse dysfunction through epigenetic and antioxidant pathways.
Why it matters
Identifying sensitive molecular biomarkers for endothelial dysfunction could improve primary cardiovascular prevention by detecting reversible vascular damage before clinical cardiovascular disease manifests.
Limits
The review provides no quantitative synthesis, effect estimates, or systematic search methodology. None of the discussed novel circulating biomarkers (endothelial microparticles, endoglin, endocan, irisin) have been validated or adopted for routine clinical practice.
Cited by
- supports Nitric oxide facilitates arterial vasodilation, decreases with aging, and is significantly depleted by high glucose levels in the bloodstream.