ArticleCirculation research2015
Effects of DNA damage in smooth muscle cells in atherosclerosis.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 citations in OpenAlex.
- Impact of adherence to the Mediterranean diet on stroke risk.GeroScience · 2025Pooled it
- Association Between Mitochondrial DNA Copy Number and Head and Neck Squamous Cell Carcinoma: A Systematic Review and Dose-Response Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
- Integrative transcriptomic and machine learning approach reveals key DDR genes and predictors of ami risk in the Bangladeshi population.Scientific reports · 2026Article
- The Pathogenic Role of the DNA Double-Stranded Breaks in Hereditary Cardiomyopathies.Heart failure clinics · 2026Review
- Decoding Vascular Senescence: Cellular Insights and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Self-DNA by Activating the CGAS-STING1 Pathway Contributes to the Pathogenesis of Atherosclerosis.Current atherosclerosis reports · 2025Review
- Premature cell senescence promotes vascular smooth muscle cell phenotypic modulation and resistance to re-differentiation.Cardiovascular research · 2025Article
- Senescence-associated alterations in histone H3 modifications, HP1 alpha levels and distribution, and in the transcriptome of vascular smooth muscle cells in different types of senescence.Cell communication and signaling : CCS · 2025Article
- Causes and consequences of DNA double-stranded breaks in cardiovascular disease.Molecular and cellular biochemistry · 2025Review
- DNA repair and disease: insights from the human DNA glycosylase NEIL family.Experimental & molecular medicine · 2025Review
- Review
- Tumor-like characteristics of vascular smooth muscle cells in atherosclerosis.Frontiers in pharmacology · 2025Review
- Athero-oncology perspective: identifying hub genes for atherosclerosis diagnosis using machine learning.Frontiers in immunology · 2025Article
- 3D confinement alters smooth muscle cell responses to chemical and mechanical cues.APL bioengineering · 2024Article
- The aging heart: exploring the role of Klotho in cardiac health/function.The journal of cardiovascular aging · 2024Article
- Atherosclerotic burden and cerebral small vessel disease: exploring the link through microvascular aging and cerebral microhemorrhages.GeroScience · 2024Review
- A cross-sectional study comparing the expression of DNA repair molecules in subjects with and without atherosclerotic plaques.Molecular biology reports · 2024Article
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- Atherosclerosis Is a Smooth Muscle Cell-Driven Tumor-Like Disease.Circulation · 2024Article
- A Concept of "Athero-Oncology": Tumor-Like Smooth Muscle Cells Drive Atherosclerosis.Circulation · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
rationaleDNA damage and the DNA damage response have been identified in human atherosclerosis, including in vascular smooth muscle cells (VSMCs). However, although double-stranded breaks (DSBs) are hypothesized to promote plaque progression and instability, in part, by promoting cell senescence, apoptosis, and inflammation, the direct effects of DSBs in VSMCs seen in atherogenesis are unknown.
objectiveTo determine the presence and effect of endogenous levels of DSBs in VSMCs on atherosclerosis. METHODS AND
resultsHuman atherosclerotic plaque VSMCs showed increased expression of multiple DNA damage response proteins in vitro and in vivo, particularly the MRE11/RAD50/NBS1 complex that senses DSB repair. Oxidative stress-induced DSBs were increased in plaque VSMCs, but DSB repair was maintained. To determine the effect of DSBs on atherosclerosis, we generated 2 novel transgenic mice lines expressing NBS1 or C-terminal deleted NBS1 only in VSMCs, and crossed them with apolipoprotein E(-/-) mice. SM22α-NBS1/apolipoprotein E(-/-) VSMCs showed enhanced DSB repair and decreased growth arrest and apoptosis, whereas SM22α-(ΔC)NBS1/apolipoprotein E(-/-) VSMCs showed reduced DSB repair and increased growth arrest and apoptosis. Accelerating or retarding DSB repair did not affect atherosclerosis extent or composition. However, VSMC DNA damage reduced relative fibrous cap areas, whereas accelerating DSB repair increased cap area and VSMC content.
conclusionsHuman atherosclerotic plaque VSMCs show increased DNA damage, including DSBs and DNA damage response activation. VSMC DNA damage has minimal effects on atherogenesis, but alters plaque phenotype inhibiting fibrous cap areas in advanced lesions. Inhibiting DNA damage in atherosclerosis may be a novel target to promote plaque stability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.