ReviewCardiovascular research2018
From genetics to response to injury: vascular smooth muscle cells in aneurysms and dissections of the ascending aorta.
Review in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 176 citations in OpenAlex.
- Mouse Models of Aortic Pathologies: Deciphering Molecular and Cellular Mechanisms from Bench to Bedside.CJC open · 2026Review
- REDD1 Silencing Aggravates Aortic Dissection and Promotes VSMC Apoptosis with Autophagy-Related Changes.Biomedicines · 2026Article
- Fibronectin-induced overactivation of αNature communications · 2026Article
- The AntioxidantAntioxidants (Basel, Switzerland) · 2026Article
- Focal adhesion proteins confer smooth muscle anoikis resistance and protection against aortic aneurysm and dissection.JCI insight · 2026Article
- A Comprehensive Review of Epigenetic Regulation of Vascular Smooth Muscle Cells During Development and Disease.Biomolecules · 2026Review
- Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026Review
- Targeting IL-1β: a potential strategy for alleviating the immunopathology of aortic aneurysms.Frontiers in immunology · 2026Review
- Lactylation Modification: From Basic Biological Process to Clinical Cardiovascular Diseases.Research (Washington, D.C.) · 2026Review
- From inflammation to remodelling: A novel BASP1Journal of advanced research · 2025Article
- Excessive glycosylation drives thoracic aortic aneurysm formation through integrated stress response.European heart journal · 2025Article
- Ascending Aortic Aneurysms: From Pathophysiology to Surgical Repair.Journal of clinical medicine · 2025Review
- The Involvement of Herpesviruses in the Pathogenesis of Thoracic Aortic Aneurysms: Passive Bystanders or Active Contributors?Reviews in cardiovascular medicine · 2025Review
- MicroRNA-15a-5p mediates abdominal aortic aneurysm progression and serves as a potential diagnostic and prognostic circulating biomarker.Communications medicine · 2025Article
- Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025Review
- Mechanisms of aortic dissection: From pathological changes to experimental andProgress in materials science · 2025Article
- Prognostic prediction of long-term survival in patients with type A aortic dissection undergoing surgical repair: development of a novel prognostic index.BMC cardiovascular disorders · 2025Article
- A multiphasic model for determination of mouse ascending thoracic aorta mass transport properties with and without aneurysm.Biomechanics and modeling in mechanobiology · 2025Article
- The innate immune axis drives aortic dissection pathogenesis through inflammation and presents novel therapeutic targets.Frontiers in immunology · 2025Review
- Modeling Thoracic Aortic Dissection Using Patient-Specific iPSCs Reveals VSMC Dysfunction and Extracellular Matrix Dysregulation.Stem cells international · 2025Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular smooth muscle cells (vSMCs) play a crucial role in both the pathogenesis of Aneurysms and Dissections of the ascending thoracic aorta (TAAD) in humans and in the associated adaptive compensatory responses, since thrombosis and inflammatory processes are absent in the majority of cases. Aneurysms and dissections share numerous characteristics, including aetiologies and histopathological alterations: vSMC disappearance, medial areas of mucoid degeneration, and extracellular matrix (ECM) breakdown. Three aetiologies predominate in TAAD in humans: (i) genetic causes in heritable familial forms, (ii) an association with bicuspid aortic valves, and (iii) a sporadic degenerative form linked to the aortic aging process. Genetic forms include mutations in vSMC genes encoding for molecules of the ECM or the TGF-β pathways, or participating in vSMC tone. On the other hand, aneurysms and dissections, whatever their aetiologies, are characterized by an increase in wall permeability leading to transmural advection of plasma proteins which could interact with vSMCs and ECM components. In this context, blood-borne plasminogen appears to play an important role, because its outward convection through the wall is increased in TAAD, and it could be converted to active plasmin at the vSMC membrane. Active plasmin can induce vSMC disappearance, proteolysis of adhesive proteins, activation of MMPs and release of TGF-β from its ECM storage sites. Conversely, vSMCs could respond to aneurysmal biomechanical and proteolytic injury by an epigenetic phenotypic switch, including constitutional overexpression and nuclear translocation of Smad2 and an increase in antiprotease and ECM protein synthesis. In contrast, such an epigenetic phenomenon is not observed in dissections. In this context, dysfunction of proteins involved in vSMC tone are interesting to study, particularly in interaction with plasma protein transport through the wall and TGF-β activation, to establish the relationship between these dysfunctions and ECM proteolysis.
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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.