ArticleEuropean heart journal2020
Prevention of aortic dissection and aneurysm via an ALDH2-mediated switch in vascular smooth muscle cell phenotype.
Article in European heart journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.
- Progress in aorta and peripheral cardiovascular disease research.Cardiovascular research · 2021Pooled it
- M1 macrophage-derived exosomal miR-155-5p exacerbates aortic dissection via SMAD5-Mediated regulation of vascular smooth muscle cell phenotype.Bioactive materials · 2026Article
- Association of ALOX12-Mediated AA/12-HETE Metabolic Dysregulation with Abdominal Aortic Aneurysm Enlargement and Dissection.Journal of cardiovascular development and disease · 2026Article
- Article
- Spatial transcriptomic analysis reveals spatial features in human Stanford type A aortic dissection.iScience · 2026Article
- GLS1 governs vascular smooth muscle cell phenotypic switching and aortic dissection via glutamate metabolism.JCI insight · 2026Article
- Integrated multi-omics analysis reveals a gut microbiota-tryptophan metabolism axis contributes to sex differences in a β-aminopropionitrile-induced aortic dissection mouse model.Biology of sex differences · 2026Article
- Targeting the Hippo pathway in pulmonary arterial hypertension: emerging pharmacological strategies.Journal of hypertension · 2026Review
- Endothelial GABA protects against aortic dissection by inhibiting endothelial and mitochondrial dysfunction and maintaining vascular homeostasis.Signal transduction and targeted therapy · 2026Article
- SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis.Nature communications · 2026Article
- Gut microbiota dysfunction mediates stress-exacerbated aortic dissection via the bacteroides vulgatus-outer membrane vesicles-stearic acid-JNK/MAPK axis.Journal of nanobiotechnology · 2026Article
- A circulating MicroRNA signature for the diagnosis of pulmonary arterial hypertension and functional characterization of candidate miR-3168.Scientific reports · 2026Article
- CircRNA-TMEM71 Inhibits Human Aortic Smooth Muscle Cell Ferroptosis and Prevents Aortic Dissection Formation Through IGF2BP3-Mediated Stability of FSP1.Journal of the American Heart Association · 2026Article
- Advanced technologies of artery-on-a-chip: a review of construction strategies and disease models.Angiogenesis · 2026Review
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- Article
- The Mechanosensation-Metabolism-Inflammation Axis: The Central Role of Piezo1 and TRPV4 in Hypertension-Related Atherosclerosis.International journal of general medicine · 2026Review
- Selenomethionine alleviates aortic dissection via PGC-1α/NRF2/TFAM-mediated mitochondrial biosynthesis against ferroptosis: an experimental study.International journal of surgery (London, England) · 2026Article
- Comparison and analysis of the diagnostic value of color doppler ultrasound and CT for abdominal aortic dissection aneurysm.Journal of cardiothoracic surgery · 2025Article
- Vascular Smooth Muscle Cell Metabolic Disorders in the Occurrence and Development of Aortic Aneurysms and Dissections: Implications for Therapy.Biomedicines · 2025Review
35 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAortic aneurysm/dissection (AAD) is a life-threatening disorder lacking effective pharmacotherapeutic remedies. Aldehyde dehydrogenase 2 (ALDH2) polymorphism is tied with various risk factors for AAD including hypertension, atherosclerosis, and hypercholesterolaemia although direct correlation between the two remains elusive. METHODS AND
resultsTwo independent case-control studies were conducted involving 307 AAD patients and 399 healthy controls in two geographically distinct areas in China. Our data revealed that subjects carrying mutant ALDH2 gene possessed a ∼50% reduced risk of AAD compared with wild-type (WT) alleles. Using 3-aminopropionitrile fumarate (BAPN)- and angiotensin II (Ang II)-induced AAD animal models, inhibition of ALDH2 was found to retard development of AAD. Mechanistically, ALDH2 inhibition ablated pathological vascular smooth muscle cell (VSMC) phenotypical switch through interaction with myocardin, a determinant of VSMC contractile phenotype. Using microarray and bioinformatics analyses, ALDH2 deficiency was found to down-regulate miR-31-5p, which further altered myocardin mRNA level. Gain-of-function and loss-of-function studies verified that miR-31-5p significantly repressed myocardin level and aggravated pathological VSMC phenotypical switch and AAD, an effect that was blunted by ALDH2 inhibition. We next noted that ALDH2 deficiency increased Max expression and decreased miR-31-5p level. Moreover, ALDH2 mutation or inhibition down-regulated levels of miR-31-5p while promoting myocardin downstream contractile genes in the face of Ang II in primary human VSMCs.
conclusionsALDH2 deficiency is associated with a lower risk of AAD in patients and mice, possibly via suppressing VSMC phenotypical switch in a miR-31-5p-myocardin-dependent manner. These findings favour a role for ALDH2 and miR-31-5p as novel targets for AAD therapy.
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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.