ArticleFrontiers in cardiovascular medicine2025
The mitochondrial dysfunction, alongside the modifiable burden of traditional risk factors, drives the development of early-onset coronary artery disease.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Replicative and Air Pollution-Induced Senescence: Telomere Dysfunction, Mitochondrial Stress, and Modulatory Effects of Astragaloside IV in Endothelial and Vascular Smooth Muscle Cells.Cardiovascular toxicology · 2026Article
- Article
- Mitochondrial Dysregulation and Molecular Signaling in Systemic Sclerosis Cardiac Disease: An Integrative Echocardiographic, Microvascular, and Biomarker Review.International journal of molecular sciences · 2026Review
- Reprogramming Atherosclerosis: Precision Drug Delivery, Nanomedicine, and Immune-Targeted Therapies for Cardiovascular Risk Reduction.Pharmaceutics · 2025Review
- Targeted drug delivery systems for atherosclerosis.Journal of nanobiotechnology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Mitochondrial dysfunction is associated with increased risk of atherosclerosis by disrupting key cellular processes that contribute to premature vascular ageing. However, the specific role of mitochondrial dysfunction in early-onset coronary artery disease (EOCAD), which is increasing at a particularly alarming rate, remains largely unexplored. This study investigated the association of leukocyte mtDNA-CN and mtDNA Methods: The study included 118 patients (99 men, 51.0 ± 5.6 years) with angiographically EOCAD (≤60 years) and 150 healthy controls (94 men, 49.8 ± 5.8 years). Quantitative RT-PCR was used to quantify mtDNA-CN and mtDNA Results: The EOCAD group had a higher prevalence of male gender ( Conclusions: EOCAD is characterized by a high prevalence of modifiable risk factors and mitochondrial damage, underscoring the need for more efforts to reduce the burden of traditional risk factors and highlighting the potential for innovative mitochondrial-targeted therapies.
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Registered trials
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