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Platelet mitochondria: the mighty few.
Ajanel, Abigail; Campbell, Robert A; Denorme, Frederik.
Affiliation
  • Ajanel A; University of Utah Molecular Medicine Program.
  • Campbell RA; Division of Microbiology and Pathology, Department Pathology.
  • Denorme F; University of Utah Molecular Medicine Program.
Curr Opin Hematol ; 30(5): 167-174, 2023 09 01.
Article in En | MEDLINE | ID: mdl-37459354
ABSTRACT
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Thrombosis / Blood Platelets Type of study: Etiology_studies / Prognostic_studies Limits: Animals / Humans Language: En Journal: Curr Opin Hematol Journal subject: HEMATOLOGIA Year: 2023 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Thrombosis / Blood Platelets Type of study: Etiology_studies / Prognostic_studies Limits: Animals / Humans Language: En Journal: Curr Opin Hematol Journal subject: HEMATOLOGIA Year: 2023 Document type: Article