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Since mitochondrial ROS contribute to cardiolipin oxidation and are controlled by antioxidants (Mari et al., 2008, 2009), mGSH arises as an important modulator of apoptotic cell death by indirectly controlling the redox state of cardiolipin (Mari et al., 2008
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This process must be tightly regulated, and the FAPs decline is essential to prevent excessive extracellular matrix deposition, impairing tissue regeneration (Mann et al., 2011)
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