PICOT alleviates myocardial ischemia-reperfusion injury by reducing intracellular levels of reactive oxygen species.

Excessive generation of reactive oxygen species is one of the main causes of myocardial ischemia-reperfusion (I/R) injury. In this study, we investigated the role of protein kinase C-interacting cousin of thioredoxin (PICOT; Grx3) during myocardial I/R using PICOT transgenic (TG) and knockdown (KD) mice. Infarction and apoptosis were attenuated in PICOT TG mice but exacerbated in PICOT KD mice upon I/R. In parallel, I/R-induced generation of was attenuated in PICOT TG mice but exacerbated in PICOT KD mice. Angiotensin II (AngII)-mediated increases in duanyu1670 and free iron levels were also attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Accordingly, H2O2-mediated cell death was attenuated in cardiomyocytes isolated from PICOT TG mice but exacerbated in cardiomyocytes from PICOT KD mice. Taken together, these data show that PICOT alleviates myocardial I/R injury by regulating intracellular duanyu1670 and free iron levels. We suggest that PICOT presents a novel therapeutic strategy for myocardial I/R injury.

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