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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
Published on: May 22, 2013
Telomere Dynamics in Cardiovascular Aging: From Molecular Mechanisms to Precision Medicine
Abbas Mohammadi1, Daniel Thomas Jones2, Somayeh Mohammadi3
1From the Department of Medicine, Valley Health System, Las Vegas, NV.
Abstract:
Telomere attrition stands as a fundamental hallmark of cardiovascular aging, driving cellular senescence and dysfunction across endothelial, cardiomyocyte, and vascular smooth muscle compartments. This review systematically examines: (1) molecular mechanisms linking telomere shortening to oxidative stress (NOX2/PRDX1 axis), epigenetic dysregulation (subtelomeric methylation, H3K9me3 loss), and mitochondrial dysfunction; (2) clinical evidence positioning leukocyte telomere length and telomere-associated proteins (eg, TRF2, POT1) as predictive biomarkers for coronary artery disease, heart failure, and hypertension; and (3) emerging therapeutic strategies ranging from telomerase activation (TA-65, GRN510) to senolytic cocktails (dasatinib + quercetin) and CRISPR (regularly interspersed short palindromic reportsclustered regularly interspaced short palindromic repeats)-based editing (6-29% efficiency in Chinese hamster ovary models). The review further addresses methodological challenges in telomere measurement (quantitative polymerase chain reaction (PCR) vs Flow-FISH standardization) and proposes an integrated risk assessment model combining leukocyte telomere length, oxidative markers (AGEs/sRAGE ratio), and epigenetic clocks. Translationally, we discuss tissue-specific delivery systems to mitigate oncogenic risks of telomerase therapies while emphasizing mitochondrial-targeted approaches for telomere stabilization. This synthesis bridges basic telomere science with clinical cardiology, offering a roadmap for personalized vascular rejuvenation strategies.
Insights
Telomere shortening drives cardiovascular aging and dysfunction. Strategies like telomerase activation and senolytics offer potential for vascular rejuvenation and personalized treatments.
Area of Science:
- Cardiovascular Aging Research
- Telomere Biology
- Molecular Cardiology
Background:
- Telomere attrition is a key factor in cardiovascular aging, leading to cellular senescence and dysfunction.
- This process affects endothelial cells, cardiomyocytes, and vascular smooth muscle.
Purpose of the Study:
- To systematically review molecular mechanisms linking telomere shortening to cardiovascular aging.
- To examine telomere length and associated proteins as biomarkers for cardiovascular diseases.
- To explore emerging therapeutic strategies for vascular rejuvenation.
Main Methods:
- Literature review of molecular mechanisms, clinical evidence, and therapeutic interventions.
- Analysis of telomere shortening links to oxidative stress, epigenetic changes, and mitochondrial dysfunction.
- Evaluation of telomere-associated proteins (TRF2, POT1) as predictive biomarkers.
Main Results:
- Telomere shortening is linked to oxidative stress (NOX2/PRDX1), epigenetic dysregulation, and mitochondrial dysfunction.
- Leukocyte telomere length and telomere proteins are predictive biomarkers for coronary artery disease, heart failure, and hypertension.
- Therapeutic strategies include telomerase activation (TA-65), senolytics (dasatinib + quercetin), and CRISPR-based editing.
Conclusions:
- Telomere attrition is a critical hallmark of cardiovascular aging with significant clinical implications.
- Emerging therapies show promise for vascular rejuvenation, but require careful consideration of risks like oncogenesis.
- An integrated risk assessment model and targeted delivery systems are proposed for personalized vascular health strategies.
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