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Defects in SDH subunits lead to succinate accumulation and oncometabolite-driven pseudohypoxia and are strongly linked to hereditary paragangliomas, pheochromocytomas and certain renal cell carcinomas, underscoring the essential role of complex II in metabolic and redox homeostasis 78,79

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This BCAC increases the activation of cytoplasmic phospholipase A2 (cPLA2) by binding to integrin 21 in platelets and promoting platelet hyperresponsiveness, thus promoting thrombosis [239]