ReviewCellular and molecular life sciences : CMLS2017
Flow signaling and atherosclerosis.
Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Stanniocalcin-1 Attenuates Cardiac Fibrosis Post Ischemia-Reperfusion Injury by Targeting the DOCKER Domain of Dedicator of Cytokinesis 1.Journal of the American Heart Association · 2026Article
- Talin1 modulates the Piezo1-YAP axis to regulate endothelial cell inflammation and atherosclerosis.Cellular and molecular life sciences : CMLS · 2025Article
- p90RSK modulates inter-and intracellular signaling in kidney diseases.Frontiers in cell and developmental biology · 2025Review
- TNIK-driven regulation of ERK5 transcriptional activity in endothelial cells.Frontiers in cardiovascular medicine · 2025Article
- Glucagon-like peptide-1 receptor agonists and the endothelium: molecular and clinical insights into cardiovascular protection.Frontiers in medicine · 2025Review
- Article
- Transcoronary Gradients of Mechanosensitive MicroRNAs as Predictors of Collateral Development in Chronic Total Occlusion.Medicina (Kaunas, Lithuania) · 2024Article
- The Role of p90 Ribosomal S6 Kinase (RSK) in Tyrosine Kinase Inhibitor (TKI)-Induced Cardiotoxicity.Journal of cardiovascular translational research · 2024Review
- Potential diagnostic markers shared between non-alcoholic fatty liver disease and atherosclerosis determined by machine learning and bioinformatic analysis.Frontiers in medicine · 2024Article
- A Data-Mining Approach to Identify NF-kB-Responsive microRNAs in Tissues Involved in Inflammatory Processes: Potential Relevance in Age-Related Diseases.International journal of molecular sciences · 2023Article
- Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.Frontiers in cardiovascular medicine · 2023Review
- Metabolic regulation of endothelial senescence.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
- Non-pharmacological interventions for vascular health and the role of the endothelium.European journal of applied physiology · 2022Review
- The regulatory roles of p53 in cardiovascular health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- The Role of Posttranslational Modification and Mitochondrial Quality Control in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2021Review
- Calciprotein Particles Cause Endothelial Dysfunction under Flow.International journal of molecular sciences · 2020Article
- Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis.Redox biology · 2020Review
- The Role of Protein SUMOylation in the Pathogenesis of Atherosclerosis.Journal of clinical medicine · 2019Review
- MAGI1 as a link between endothelial activation and ER stress drives atherosclerosis.JCI insight · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis rarely develops in the region of arteries exposed to undisturbed flow (u-flow, unidirectional flow). Instead, atherogenesis occurs in the area exposed to disturbed flow (d-flow, multidirectional flow). Based on these general pathohistological observations, u-flow is considered to be athero-protective, while d-flow is atherogenic. The fact that u-flow and d-flow induce such clearly different biological responses in the wall of large arteries indicates that these two types of flow activate each distinct intracellular signaling cascade in vascular endothelial cells (ECs), which are directly exposed to blood flow. The ability of ECs to differentially respond to the two types of flow provides an opportunity to identify molecular events that lead to endothelial dysfunction and atherosclerosis. In this review, we will focus on various molecular events, which are differentially regulated by these two flow types. We will discuss how various kinases, ER stress, inflammasome, SUMOylation, and DNA methylation play roles in the differential flow response, endothelial dysfunction, and atherosclerosis. We will also discuss the interplay among the molecular events and how they coordinately regulate flow-dependent signaling and cellular responses. It is hoped that clear understanding of the way how the two flow types beget each unique phenotype in ECs will lead us to possible points of intervention against endothelial dysfunction and cardiovascular diseases.
Indexed as
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What OpenQuestion holds
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.