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Following the compete transection of the quadriceps muscle in rats, a traumatic definitive defect under normal healing conditions would not be compensated (Staresinic et al

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Importantly, both the collapse of m and arrhythmias are blocked by ligands of the mBzR complex, and not by cyclosporine A, the classical permeability transition pore (PTP) inhibitor, indicating a graded redox sensitivity of the target mitochondrial ion channels [6, 7]