Platelet mitochondria: the mighty few

被引:9
作者
Ajanel, Abigail [1 ,2 ]
Campbell, Robert A. [1 ,2 ,3 ]
Denorme, Frederik [1 ,4 ,5 ]
机构
[1] Univ Utah, Mol Med Program, Salt Lake City, UT USA
[2] Univ Utah, Dept Pathol, Div Microbiol & Pathol, Salt Lake City, UT USA
[3] Univ Utah, Dept Internal Med, Div Hematol, Salt Lake City, UT USA
[4] Univ Utah, Dept Neurol, Div Vasc Neurol, Salt Lake City, UT USA
[5] Univ Utah Hlth Sci Ctr, Eccles Inst Human Genet, 15 North 2030East,Bldg 533, Salt Lake City, UT 84112 USA
关键词
arterial thrombosis; diabetes; mitochondria; oxidative stress; platelets; PERMEABILITY TRANSITION PORE; LOW-DENSITY-LIPOPROTEIN; CYCLOPHILIN-D; GLUCOSE; CALCIUM; METABOLISM; AGGREGATION; ACTIVATION; THROMBIN; CA2+;
D O I
10.1097/MOH.0000000000000772
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of reviewPlatelet 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 findingsIncreasing 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.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.
引用
收藏
页码:167 / 174
页数:8
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