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Updated: May 12, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro

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Published on: June 2, 2022

Aging and coronary artery calcification: a Mendelian randomization study.

Mateusz Lejawa¹, Marcin Goławski¹, Mateusz Olek¹

¹Department of Pharmacology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Poland.

Archives of Medical Science : AMS

|May 11, 2026

Summary

Longer telomere length (TL) is causally linked to reduced coronary artery calcification (CAC), suggesting TL protects against atherosclerosis. Other aging markers like epigenetic age and dental health did not show a significant causal link with CAC.

Keywords:

Mendelian randomization biological aging coronary artery calcification epigenetic aging telomere length

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Published on: May 31, 2016

Area of Science:

Cardiovascular Research
Genetics
Aging Biology

Background:

Coronary artery calcification (CAC) is a key indicator of atherosclerosis and cardiovascular disease (CVD) risk.
While associated with chronological aging, CAC's role as a marker of biological aging is not fully understood.
Telomere length (TL), epigenetic aging, and dental health are proposed biological aging indicators, but their association with CAC requires investigation.

Purpose of the Study:

To investigate the potential causal relationship between telomere length (TL), epigenetic aging markers, and dental deterioration with coronary artery calcification (CAC).
To determine if these biological aging indicators can serve as reliable biomarkers for vascular aging and atherosclerosis progression.

Main Methods:

Utilized two-sample and three-sample Mendelian randomization (MR) analyses.
Employed summary-level statistics from large-scale genome-wide association studies (GWASs).
Assessed causal effects of genetic liability for TL, intrinsic epigenetic age acceleration (IEAA), phenotypic age (PhenoAge), and dental deterioration on CAC.

Main Results:

Genetically determined longer TL showed a significant inverse causal association with lower CAC levels (IVW p < 0.001).
Robustness of the TL-CAC association confirmed through MR-Egger (p = 0.03) and weighted median (WME) analyses (p = 0.004).
No significant causal relationships were found between epigenetic aging markers (IEAA, PhenoAge) or dental deterioration traits and CAC.

Conclusions:

This study provides evidence for an inverse causal relationship between TL and CAC, supporting CAC as a biomarker of biological aging.
Epigenetic aging markers and dental deterioration parameters were not found to be causally associated with CAC.
Further research is needed to explore additional aging traits and refine genetic instruments for epigenetic aging and dental health in the context of vascular aging.