ArticleCardiovascular drugs and therapy2013
Inhibition of platelet activation by clopidogrel prevents hypertension-induced cardiac inflammation and fibrosis.
Article in Cardiovascular drugs and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.
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- Drugs for treating myocardial fibrosis.Frontiers in pharmacology · 2023Review
- P2Y12 inhibitor clopidogrel inhibits renal fibrosis by blocking macrophage-to-myofibroblast transition.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Clopidogrel delays and can reverse diabetic nephropathy pathogenesis in type 2 diabeticWorld journal of diabetes · 2022Article
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- Cardiac inflammation and fibrosis following chemo/radiation therapy: mechanisms and therapeutic agents.Inflammopharmacology · 2022Review
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- The probable role and therapeutic potential of the PI3K/AKT signaling pathway in SARS-CoV-2 induced coagulopathy.Cellular & molecular biology letters · 2022Review
- The Therapeutic Potential of Anticoagulation in Organ Fibrosis.Frontiers in medicine · 2022Review
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9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePlatelets are essential for primary hemostasis; however, platelet activation also plays an important proinflammatory role. Inflammation promotes the development of cardiac fibrosis and heart failure induced by hypertension. In this study, we aimed to determine whether inhibiting platelet activation using clopidogrel could inhibit hypertension-induced cardiac inflammation and fibrosis.
methodsUsing a mouse model of angiotensin II (Ang II) infusion (1,500 ng/[kg·min] for 7 days), we determined the role of platelet activation in Ang II infusion-induced cardiac inflammation and fibrosis using a P2Y12 receptor inhibitor, clopidogrel (50 mg/[kg·day]).
resultsCD41 staining showed that platelets accumulated in Ang II-infused hearts. Clopidogrel treatment inhibited Ang II infusion-induced accumulation of α-SMA(+) myofibroblasts and cardiac fibrosis (4.17 ± 1.26 vs. 1.46 ± 0.81, p < 0.05). Infiltration of inflammatory cells, including Mac-2(+) macrophages and CD45(+)Ly6G(+) neutrophils (30.38 ± 4.12 vs. 18.7 ± 2.38, p < 0.05), into Ang II-infused hearts was also suppressed by platelet inhibition. Real-time PCR and immunohistochemical staining showed that platelet inhibition significantly decreased the expression of interleukin-1β and transforming growth factor-β. Acute injection of Ang II or PE stimulated platelet activation and platelet-leukocyte conjugation, which were abolished by clopidogrel treatment.
conclusionThus, inhibition of platelet activation by clopidogrel prevents cardiac inflammation and fibrosis in response to Ang II. Taken together, our results indicate Ang II infusion-induced hypertension stimulated platelet activation and platelet-leukocyte conjugation, which initiated inflammatory responses that contributed to cardiac fibrosis.
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