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H2/3-RLXs antifibrotic effect is mediated by the induction of MMP-1 and MMP-13 and enzymatic degradation of collagens (214)

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However, more recent studies assessing the role of ferrous iron in the pathophysiology first in vitro [74, 75] and then in vivo [76, 77] provided evidence that after a toxic dose of APAP ferrous iron derived from lysosomes is taken up into mitochondria through a Ca 2+ uniporter and facilitates the MPTP opening and cell death