ReviewArteriosclerosis, thrombosis, and vascular biology2014
Novel mechanisms of endothelial mechanotransduction.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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.
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Who cites it
63 citing papers in PubMed.
- Article
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.Cells · 2025Review
- Aortic Stenosis Prevention: Is a New Cardiovascular Disease Paradigm Coming of Age?Journal of clinical medicine · 2025Review
- Exploring the Revolutionary Impact of YAP Pathways on Physical and Rehabilitation Medicine.Biomolecules · 2025Review
- Vascular Endothelium in Health and Disease: Structure, Function, Assessment and Role in Metabolic Disorders.Vascular health and risk management · 2025Review
- Polycomb Repressive Complex 2 promotes atherosclerotic plaque vulnerability.bioRxiv : the preprint server for biology · 2024Article
- Endothelial KDM5B Regulated by Piezo1 Contributes to Disturbed Flow Induced Atherosclerotic Plaque Formation.Journal of cellular and molecular medicine · 2024Article
- Article
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis.Nature cardiovascular research · 2024Article
- The roles of Hippo/YAP signaling pathway in physical therapy.Cell death discovery · 2024Review
- Gamma protocadherins in vascular endothelial cells inhibit Klf2/4 to promote atherosclerosis.bioRxiv : the preprint server for biology · 2024Article
- Marginated aberrant red blood cells induce pathologic vascular stress fluctuations in a computational model of hematologic disorders.Science advances · 2023Article
- Flow-induced reprogramming of endothelial cells in atherosclerosis.Nature reviews. Cardiology · 2023Review
- Insulin Resistance and Hypertension: Mechanisms Involved and Modifying Factors for Effective Glucose Control.Biomedicines · 2023Review
- The Action of Angiocrine Molecules Sourced from Mechanotransduction-Related Endothelial Cell Partially Explain the Successful of Titanium in Osseointegration.Journal of functional biomaterials · 2023Article
- Marginated aberrant red blood cells induce pathologic vascular stress fluctuations in a computational model of hematologic disorders.bioRxiv : the preprint server for biology · 2023Article
- Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.Frontiers in cardiovascular medicine · 2023Review
- Endothelial activation and fibrotic changes are impeded by laminar flow-induced CHK1-SENP2 activity through mechanisms distinct from endothelial-to-mesenchymal cell transition.Frontiers in cardiovascular medicine · 2023Article
3 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
2 authors.
Funding
Abstract
Atherosclerosis is a focal disease that develops preferentially where nonlaminar, disturbed blood flow occurs, such as branches, bifurcations, and curvatures of large arteries. Endothelial cells sense and respond differently to disturbed flow compared with steady laminar flow. Disturbed flow that occurs in so-called atheroprone areas activates proinflammatory and apoptotic signaling, and this results in endothelial dysfunction and leads to subsequent development of atherosclerosis. In contrast, steady laminar flow as atheroprotective flow promotes expression of many anti-inflammatory genes, such as Kruppel-like factor 2 and endothelial nitric oxide synthase and inhibits endothelial inflammation and athrogenesis. Here we will discuss that disturbed flow and steady laminar flow induce pro- and antiatherogenic events via flow type-specific mechanotransduction pathways. We will focus on 5 mechanosensitive pathways: mitogen-activated protein kinases/extracellular signal-regulated kinase 5/Kruppel-like factor 2 signaling, extracellular signal-regulated kinase/peroxisome proliferator-activated receptor signaling, and mechanosignaling pathways involving SUMOylation, protein kinase C-ζ, and p90 ribosomal S6 kinase. We think that clarifying regulation mechanisms between these 2 flow types will provide new insights into therapeutic approaches for the prevention and treatment of atherosclerosis.
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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.