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Aubert P, Andre J, Dallemagne MJ, et al

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This mechanism establishes OLA as a promising anti-fibrotic therapeutic candidate ( Mitochondria-targeted antioxidants or CYP2E1 inhibition prevents this toxicity, highlighting CcO dysfunction as a key pathological mechanism ( Daphnia magna through its reactive metabolite NAPQI

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moreover, increased GGT levels correlated with BMPR2 mutation, hemodynamic dysfunction, and poor outcomes in male patients with idiopathic pulmonary arterial hypertension [77]

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