Telomere Length Emerges as Key Biomarker for Heart Disease Risk

Telomere shortening has emerged as a fundamental driver of cardiovascular aging, offering new insights into heart disease prevention and treatment. This comprehensive review examines how telomere attrition leads to cellular senescence across critical heart tissues including endothelial cells, cardiomyocytes, and vascular smooth muscle.

The researchers analyzed molecular mechanisms connecting telomere shortening to cardiovascular dysfunction. Key pathways include oxidative stress through the NOX2/PRDX1 axis, epigenetic dysregulation involving subtelomeric methylation and H3K9me3 loss, and mitochondrial dysfunction. These processes collectively accelerate cardiovascular aging and disease progression.

Clinical evidence demonstrates that leukocyte telomere length and telomere-associated proteins like TRF2 and POT1 serve as predictive biomarkers for major cardiovascular conditions including coronary artery disease, heart failure, and hypertension. This positions telomere measurement as a valuable clinical tool for risk assessment.

Emerging therapeutic strategies show promise for cardiovascular rejuvenation. These include telomerase activators like TA-65 and GRN510, senolytic drug combinations such as dasatinib plus quercetin, and CRISPR-based gene editing approaches achieving 6-29% efficiency in laboratory models. The review addresses methodological challenges in telomere measurement and proposes tissue-specific delivery systems to minimize oncogenic risks.

The authors recommend an integrated risk assessment model combining leukocyte telomere length, oxidative stress markers, and epigenetic clocks for personalized cardiovascular medicine. This approach bridges fundamental telomere science with clinical cardiology practice.