ReviewThrombosis journal2019
Protease-activated receptors (PARs): mechanisms of action and potential therapeutic modulators in PAR-driven inflammatory diseases.
Review in Thrombosis journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 216 papers, 3 of them syntheses that pooled it.
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
216 citing papers in PubMed, 3 syntheses or guidelines pooled it, 360 citations in OpenAlex.
- Paneth Cells: Recent Updates on Elucidating Therapeutic Implications in Gastroenterological Disease Management.Current medicinal chemistry · 2025Pooled it
- Pathological mechanisms and future therapeutic directions of thrombin in intracerebral hemorrhage: a systematic review.Frontiers in pharmacology · 2024Pooled it
- COVID-19-Associated acute respiratory distress syndrome (CARDS): Mechanistic insights on therapeutic intervention and emerging trends.International immunopharmacology · 2021Pooled it
- The Role of Skin Surface pH in Age Associated Pruritus: Mechanistic and Clinical Insights.American journal of clinical dermatology · 2026Review
- Insomnia-Associated Circadian and Thrombotic Alterations Coincide with Morning Cardiac Vulnerability.ACS pharmacology & translational science · 2026Article
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Review
- Textilinin-1, a Snake Venom-Derived Kunitz-Type Protease Inhibitor, Accelerates Wound Healing Through Anti-Inflammatory, Antibacterial, and Pro-Regenerative Activities.Pharmaceutics · 2026Article
- Critical role of keratinocytes and protease-activated receptor 2 in secondary lymphedema development.Clinical and translational medicine · 2026Article
- Integrated Proteomics and Metabolomics Analysis Reveals Potential Pathways Underlying Onion-Mediated Regulation of Spleen Immune Function in Liangshan Black Sheep.Veterinary sciences · 2026Article
- PAR2-β-arrestin 2-ERK axis mediatesiScience · 2026Article
- Sepsis-triggered proteolysis of profibrinolytic annexin A2 associated with microvasculopathy-related organ dysfunction.Blood vessels, thrombosis & hemostasis · 2026Article
- Modulatory Effects of Dabigatran on PAR-1 Activity and Viability in Adipose-Derived Mesenchymal Stem Cells.International journal of molecular sciences · 2026Article
- Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of the Coagulation Factor Xa-Protease-Activated Receptor-1 Signaling Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Targeting PAR-2 with a negative allosteric modulator increases tumor antigen presentation and potentiates anti-PD-1 immunotherapy.Journal for immunotherapy of cancer · 2026Article
- Protease-Activated Receptor-2 Promotes Metastasis: An Emerging Therapeutic Target.Molecular cancer research : MCR · 2026Review
- PAR-1 in Alzheimer's Disease: Pathophysiological Insights and Mechanistic Perspectives.Current medical science · 2026Review
- IGSF9 drives malignant transformation and predicts early-stage lung adenocarcinoma in integrated transcriptomic analyses.Discover oncology · 2026Article
- Identifying microbial protease allergens through protein language model-guided homology.Cell systems · 2026Article
- Long-chain polyphosphates induce glomerular microthrombi and exacerbate LPS-induced acute kidney injury in mouse.Disease models & mechanisms · 2026Article
156 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory diseases have become increasingly prevalent with industrialization. To address this, numerous anti-inflammatory agents and molecular targets have been considered in clinical trials. Among molecular targets, protease-activated receptors (PARs) are abundantly recognized for their roles in the development of chronic inflammatory diseases. In particular, several inflammatory effects are directly mediated by the sensing of proteolytic activity by PARs. PARs belong to the seven transmembrane domain G protein-coupled receptor family, but are unique in their lack of physiologically soluble ligands. In contrast with classical receptors, PARs are activated by N-terminal proteolytic cleavage. Upon removal of specific N-terminal peptides, the resulting N-termini serve as tethered activation ligands that interact with the extracellular loop 2 domain and initiate receptor signaling. In the classical pathway, activated receptors mediate signaling by recruiting G proteins. However, activation of PARs alternatively lead to the transactivation of and signaling through receptors such as co-localized PARs, ion channels, and toll-like receptors. In this review we consider PARs and their modulators as potential therapeutic agents, and summarize the current understanding of PAR functions from clinical and in vitro studies of PAR-related inflammation.
Identifiers
What Socratic 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 Socratic graph.