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Analysis of transcript expression showed that the highest level of mutant transcript was in skeletal muscle (80%), while liver and heart had lower levels (46 and 30%, respectively), explaining the tissue specific phenotype of this disease [12]

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10.1016/s0891-5849(98)00202-0 161 PaulS.NaharA.BhagawatiM.KunwarA

Pathological mediators like inducible nitric oxide synthase (iNOS) and hydrogen peroxide (H 2 O 2 ) impair the electron transport chain in M1 macrophages, leading to mitochondrial dysfunction and excessive accumulation of reactive oxygen species (ROS) and mitochondrial ROS (mtROS), which amplify inflammatory cascades and exacerbate oxidative stress [15,16,17]

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