ArticleCardiology2017
Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation.
Article in Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- Thromboinflammation is associated with clinical outcome after ST-elevation myocardial infarction.Blood advances · 2024Observational
- Clonal hematopoiesis is associated with cardiovascular events in patients with stable coronary artery disease.iScience · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- Article
- Thrombin-mediated activation of PAR1 enhances doxorubicin-induced cardiac injury in mice.Blood advances · 2023Article
- Serum protease-activated receptor (PAR-1) levels as a potential biomarker for diagnosis of inflammation in type 2 diabetic patients.Inflammopharmacology · 2022Article
- Plasma C4 level was associated with mortality, cardiovascular and cerebrovascular complications in hemodialysis patients.BMC nephrology · 2022Article
- Enhanced Thrombin Generation Is Associated with Worse Left Ventricular Scarring after ST-Segment Elevation Myocardial Infarction: A Cohort Study.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cardioprotection by direct factor Xa inhibition in angiotensin II overexpression.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Thrombin Inhibition Prevents Endothelial Dysfunction and Reverses 20-HETE Overproduction without Affecting Blood Pressure in Angiotensin II-Induced Hypertension in Mice.International journal of molecular sciences · 2021Article
- COVID-19 and metabolic comorbidities: An update on emerging evidences for optimal therapies.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- Review
- A novel mechanism of ACE inhibition-associated enhanced platelet reactivity: disproof of the ARB-MI paradox?European journal of clinical pharmacology · 2020Article
- Blockade of PAR-1 Signaling Attenuates Cardiac Hypertrophy and Fibrosis in Renin-Overexpressing Hypertensive Mice.Journal of the American Heart Association · 2020Article
- Searching therapeutic strategy of new coronavirus pneumonia from angiotensin-converting enzyme 2: the target of COVID-19 and SARS-CoV.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Review
- Cell type-specific mechanisms coupling protease-activated receptor-1 to infectious colitis pathogenesis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Using PAR4 Inhibition as an Anti-Thrombotic Approach: Why, How, and When?International journal of molecular sciences · 2019Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAngiotensin II (Ang II) plays an important role in cardiovascular disease. It also leads to the activation of coagulation. The coagulation protease thrombin induces cellular responses by activating protease-activated receptor 1 (PAR-1). We investigated whether PAR-1 contributes to Ang II-induced cardiovascular remodeling and inflammation. METHODS AND
resultsPAR-1+/+ (wild-type; WT) and PAR-1-/- mice were infused with Ang II (600 ng/kg/min) for up to 4 weeks. In WT mice, this dose of Ang II did not cause a significant increase in blood pressure but it did cause pathological changes in both the aorta and the heart. Ang II infusion resulted in vascular remodeling of the aorta, demonstrated by a significant increase in medial wall thickening and perivascular fibrosis. Importantly, both parameters were significantly attenuated by PAR-1 deficiency. Furthermore, perivascular fibrosis around coronary vessels was reduced in Ang II-treated PAR-1-/- mice compared to WT mice. In addition, PAR-1 deficiency significantly attenuated Ang II induction of inflammatory cytokines and profibrotic genes in the aortas compared to WT mice. Finally, PAR-1 deficiency had no effect on Ang II-induced heart hypertrophy. However, the heart function measured by fractional shortening was less impaired in PAR-1-/- mice than in WT mice.
conclusionOur data indicate that PAR-1 plays a significant role in cardiovascular remodeling mediated by a blood pressure-independent action of Ang II.
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Registered trials
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