ArticleJournal of molecular and cellular cardiology2018
Protease-activated receptor 1 activation enhances doxorubicin-induced cardiotoxicity.
Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Akkermansia muciniphila ameliorates doxorubicin-induced cardiotoxicity by regulating PPARα-dependent mitochondrial biogenesis.NPJ biofilms and microbiomes · 2025Article
- Review
- Biased agonism of protease-activated receptor-1 regulates thromboinflammation in murine sickle cell disease.Blood advances · 2024Article
- Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing.Cell research · 2023Article
- Thrombin-mediated activation of PAR1 enhances doxorubicin-induced cardiac injury in mice.Blood advances · 2023Article
- Non-Coding RNAs in Cell-to-Cell Communication: Exploiting Physiological Mechanisms as Therapeutic Targets in Cardiovascular Pathologies.International journal of molecular sciences · 2023Review
- Mechanisms and Drug Intervention for Doxorubicin-Induced Cardiotoxicity Based on Mitochondrial Bioenergetics.Oxidative medicine and cellular longevity · 2022Review
- Cardiotoxicity of Cancer Treatments: Focus on Anthracycline Cardiomyopathy.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- Periplocymarin Alleviates Doxorubicin-Induced Heart Failure and Excessive Accumulation of Ceramides.Frontiers in cardiovascular medicine · 2021Article
- Novel Mechanisms of Anthracycline-Induced Cardiovascular Toxicity: A Focus on Thrombosis, Cardiac Atrophy, and Programmed Cell Death.Frontiers in cardiovascular medicine · 2021Review
- Exosomal LncRNA-NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p.Journal of nanobiotechnology · 2020Article
- Thrombin activation of PAR-1 contributes to microvascular stasis in mouse models of sickle cell disease.Blood · 2020Article
- R-(-)-carvone Attenuated Doxorubicin Induced CardiotoxicityBalkan medical journal · 2020Article
- High CSF thrombin concentration and activity is associated with an unfavorable outcome in patients with intracerebral hemorrhage.PloS one · 2020Article
- Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Protease-activated receptor 4 protects mice from Coxsackievirus B3 and H1N1 influenza A virus infection.Cellular immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveThe anti-cancer anthracycline drug Doxorubicin (Dox) causes cardiotoxicity. We investigated the role of protease-activated receptor 1 (PAR-1) in Dox-induced cardiotoxicity. METHODS AND
resultsIn vitro experiments revealed that PAR-1 enhanced Dox-induced mitochondrial dysfunction, reactive oxygen species and cell death of cardiac myocytes and cardiac fibroblasts. The contribution of PAR-1 to Dox-induced cardiotoxicity was investigated by subjecting PAR-1
conclusionOur results indicate that activation of PAR-1 contributes to Dox-induced cardiotoxicity. Inhibition of PAR-1 may be a new approach to reduce Dox-induced cardiotoxicity in cancer patients.
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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.