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Excess ROS can damage all major cellular constituents (DNA, proteins, and lipids) and even lead to cell death, apoptosis, hypertrophy, fibrosis, and contractile dysfunction in the myocardium [8, 11]

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Inhibition of HIF-1 ameliorates pulmonary fibrosis by suppressing M2 macrophage polarization through PRMT1/STAT6 signals

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