ArticleNature communications2024
Aging aggravates aortic aneurysm and dissection via miR-1204-MYLK signaling axis in mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Vascular Smooth Muscle Cell Plasticity in Atherosclerosis: Mechanisms, Recent Advances, and Therapeutic Implications.Reviews in cardiovascular medicine · 2026Review
- Genetic and molecular mechanisms of hereditary thoracic aortic aneurysm and dissection (Review).Molecular medicine reports · 2026Review
- Erosion or Explosion: Integrated Single-Cell Transcriptomics Reveals Cellular Heterogeneity in Aortic Aneurysm and Dissection.Inflammation · 2026Article
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Early Outcomes After Total Arch Replacement With Frozen Elephant Trunk in Elderly Patients With Acute Type A Aortic Dissection.Aging medicine (Milton (N.S.W)) · 2026Article
- Mortality trends and disparities associated with aortic aneurysm and aortic dissection in the United States from 1999 to 2023: a CDC WONDER database analysis.BMC cardiovascular disorders · 2026Article
- Spatiotemporal Mortality Patterns and Temperature-Associated Risk of Aortic Dissection in the United States: A National CDC WONDER Database Analysis.Vascular health and risk management · 2026Article
- High density-lipoprotein regulates liquid-liquid phase separation of heat shock protein β-1 by lncRNA HDRACA to affect vascular inflammation and atherosclerosis.International journal of biological sciences · 2026Article
- Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Vascular Smooth Muscle Cell Metabolic Disorders in the Occurrence and Development of Aortic Aneurysms and Dissections: Implications for Therapy.Biomedicines · 2025Review
- [Identification and Underlying Mechanisms of Immune Cell- and Senescence-Related Biomarkers in Atrial Fibrillation].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Review
- Using RNA therapeutics to promote healthy aging.Nature aging · 2025Review
- Analysis of Nicotine Toxicity and Mechanisms of Senescence in Nucleus Pulposus Cells Using Network Toxicology and Molecular Docking Technique.JOR spine · 2025Article
- Apolipoprotein A-I Mimetic Peptide Restores VEGF-induced Angiogenesis in Hypercholesterolemic Ischemic Heart by Reducing HDL Proinflammatory Properties.Journal of cardiovascular translational research · 2025Article
- Association of triglyceride-glucose index and its combination with obesity indicators in predicting the risk of aortic aneurysm and dissection.Frontiers in nutrition · 2024Article
- A preliminary study of sirtuin-1 on angiotensin II-induced senescence and inflammation in abdominal aortic aneurysms.CytoJournal · 2024Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 participants were recruited for the screening of differentially expressed plasma microRNAs (miRNAs). We found that miR-1204 is significantly increased in both the plasma and aorta of elder patients with AAD and is positively correlated with age. Cell senescence induces the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induces vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. Furthermore, miR-1204 aggravates angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuates β-aminopropionitrile monofumarate-induced AAD development in mice. Mechanistically, miR-1204 directly targets myosin light chain kinase (MYLK), leading to the acquisition of a senescence-associated secretory phenotype (SASP) by VSMCs and loss of their contractile phenotype. MYLK overexpression reverses miR-1204-induced VSMC senescence, SASP and contractile phenotypic changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest that aging aggravates AAD via the miR-1204-MYLK signaling axis.
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