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Nitric oxide generated by activated inducible Nitric oxide synthase reacts with specific cysteine residues (e.g., Cys166) of ERO1 which leads to the S-nitrosylation of ERO1 and reduces the production of oxidants in the ER, thus causing ER reducing stress and finally promoting the aging process of cells ( ERO1 may be a potential therapeutic target in hereditary myopathies ( 2+ dynamics between ER and mitochondria, and subsequently affecting muscle cell bioenergetics and muscle contractile function
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Treated tendons demonstrate better organized collagen fibers and superior biomechanical properties compared to naturally healed controls
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