ReviewCurrent opinion in hematology2016
Integration of endothelial protease-activated receptor-1 inflammatory signaling by ubiquitin.
Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 40 citations in OpenAlex.
- Pulmonary arterial hypertension induces a metabolic and inflammatory hepatopathy.The Journal of clinical investigation · 2026Article
- Pulmonary Arterial Hypertension Induces a Metabolic and Inflammatory Hepatopathy.bioRxiv : the preprint server for biology · 2026Article
- Active Endothelial Inactivation of Hyperpermeability: The Role of Nitric Oxide-Driven cAMP/Epac1 Signaling.Journal of cardiovascular development and disease · 2025Review
- Enzyme-Based Anti-Inflammatory Therapeutics for Inflammatory Diseases.Pharmaceutics · 2025Review
- Structural basis for the activation of proteinase-activated receptors PAR1 and PAR2.Nature communications · 2025Article
- Targeting PAR-2-driven inflammatory pathways in colorectal cancer: mechanistic insights from atorvastatin and rosuvastatin treatment in cell line models.Translational cancer research · 2025Article
- Endothelial protease-activated receptor 4: impotent or important?Frontiers in cardiovascular medicine · 2025Review
- Acetaminophen Overdose Reveals PAR4 as a Low-Expressing but Potent Receptor on the Hepatic Endothelium in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- The immunomodulatory and antitumor properties of the bacterial metalloprotease Oligopeptidase A are mediated by TLR4/MyD88/TRIF and MAPK signaling pathways.Frontiers in immunology · 2025Article
- Rivaroxaban as a Protector of Oxidative Stress-Induced Vascular Endothelial Glycocalyx Damage via the IQGAP1/PAR1-2/PI3K/Akt Pathway.Journal of vascular research · 2025Article
- Acetaminophen Overdose Reveals Protease-Activated Receptor 4 as a Low-Expressing but Potent Receptor on the Hepatic Endothelium.bioRxiv : the preprint server for biology · 2024Article
- Unraveling the Molecular Mechanisms of Activated Protein C (APC) in Mitigating Reperfusion Injury and Cardiac Ischemia: a Promising Avenue for Novel Therapeutic Interventions.Journal of cardiovascular translational research · 2024Review
- Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing.Cell research · 2023Article
- Endothelial PAR2 activation evokes resistance artery relaxation.Journal of cellular physiology · 2023Article
- A mast cell-thermoregulatory neuron circuit axis regulates hypothermia in anaphylaxis.Science immunology · 2023Article
- Distinct pleiotropic effects of direct oral anticoagulants on cultured endothelial cells: a comprehensive review.Frontiers in pharmacology · 2023Review
- Vasculopathy in COVID-19.Blood · 2022Review
- Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021Review
- Role of endothelial cell receptors in the context of SARS-CoV-2 infection (COVID-19).Proceedings (Baylor University. Medical Center) · 2021Article
- Extracellular Vesicles and Alveolar Epithelial-Capillary Barrier Disruption in Acute Respiratory Distress Syndrome: Pathophysiological Role and Therapeutic Potential.Frontiers in physiology · 2021Review
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 at 1 institution in 1 country.
Funding
Abstract
purpose of reviewThe maintenance and integrity of the endothelial barrier is essential for vascular homeostasis. Endothelial barrier dysfunction is mediated by various inflammatory factors, many of which act through G protein-coupled receptors including protease-activated receptors (PARs). PARs are expressed in multiple cell types in the vasculature and mediate cellular responses to thrombin, the key effector protease of the coagulation cascade. Thrombin activation of PAR1 induces endothelial barrier permeability through multiple pathways. Here, we discuss the mechanism by which thrombin activation of PAR1 promotes endothelial barrier breakdown and highlight recent advances that have provided new insight into molecular mechanisms that control endothelial barrier integrity. RECENT
findingsAlthough the signal transduction pathways induced by thrombin activation of PAR1 in endothelial cells have been extensively studied, the key regulatory mechanisms remain poorly understood. Posttranslational modifications are integral to the regulation of PAR1 signaling and recent studies suggest a novel function for ubiquitination of PAR1 in regulation of endothelial barrier permeability. SUMMARY: An understanding of how endothelial barrier permeability is regulated by thrombin activation of PAR1 is important for the discovery of new drug targets that can be manipulated to control endothelial barrier permeability and prevent progression of vascular inflammation.
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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.