血小板
氧化应激
线粒体
止血
活性氧
血栓形成
抗血栓
血脂异常
医学
糖尿病
血小板活化
生物信息学
药理学
内科学
生物
细胞生物学
内分泌学
作者
Abigail Ajanel,Robert A. Campbell,Frederik Denorme
出处
期刊:Current Opinion in Hematology
[Ovid Technologies (Wolters Kluwer)]
日期:2023-07-17
卷期号:30 (5): 167-174
被引量:2
标识
DOI:10.1097/moh.0000000000000772
摘要
Purpose of review Platelet mitochondrial dysfunction is both caused by, as well as a source of oxidative stress. Oxidative stress is a key hallmark of metabolic disorders such as dyslipidemia and diabetes, which are known to have higher risks for thrombotic complications. Recent findings Increasing evidence supports a critical role for platelet mitochondria beyond energy production and apoptosis. Mitochondria are key regulators of reactive oxygen species and procoagulant platelets, which both contribute to pathological thrombosis. Studies targeting platelet mitochondrial pathways have reported promising results suggesting antithrombotic effects with limited impact on hemostasis in animal models. Summary Targeting platelet mitochondria holds promise for the reduction of thrombotic complications in patients with metabolic disorders. Future studies should aim at validating these preclinical findings and translate them to the clinic.
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