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Vaishnava, S

While the molecular mechanisms of APAP hepatotoxicity are diverse and include different players, including innate immune response, in this review we will focus on the mitochondriallysosomal axis, which has emerged as a novel liason in several pathologies, including lysosomal storage diseases (Torres et al., 2017a), to pinpoint its role in APAP-mediated hepatotoxicity

These factors include the amyloid-beta (A) cascade hypothesis, hyperphosphorylation of Tau protein, cholinergic dysfunction, neuroinflammatory responses, and excitotoxicity of the glutamate system

The arginineproline metabolic network plays a central role in sustaining fibroblast activation, ECM overproduction, and oxidative stress in pulmonary fibrosis

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