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In contrast, mutation of the C-terminal active site cysteine increases the activity of GLRX, presumably by preventing disulfide bond formation between the two active site cysteines 20,21 , and renders GLRX a monothiol enzyme only capable of catalysis of (de)glutathionylation 22

Leukocytes, particularly neutrophils and monocyte-derived macrophages, are major players in wound healing [108]

Dihydroartemisinin inhibits angiogenesis in breast cancer via regulating VEGF and MMP-2/-9

10.1007/978-94-017-9511-1_30 [DOI] [Google Scholar] Liu J.-H., Zhang R.-R., Peng X.-R., Ding Z.-T., Qiu M.-H

Our findings indicate that the molecular mechanisms of oxidative stress have been more thoroughly investigated, underscoring its scientific and clinical importance in understanding disease development and potential interventions

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