Publications by authors named "Adrien Kleindienst"
Article Synopsis
- The study explores how oxidative stress affects cardiac function by investigating the interaction between β-adrenergic signaling and redox signaling on key proteins involved in heart contraction.
- High levels of oxidative stress led to harmful changes in regulatory proteins (MyBP-C and TnI) and resulted in decreased heart function, while moderate exercise stress improved cardiac function by enhancing protein phosphorylations.
- Treatment with N-acetylcysteine (NAC) showed potential in reversing oxidative damage and restoring normal cardiac function under high stress conditions, highlighting the crucial role of these signaling pathways in heart health.
Obesity and diabetes are associated with higher cardiac vulnerability to ischemia-reperfusion (IR). The cardioprotective effect of regular exercise has been attributed to β3-adrenergic receptor (β3AR) stimulation and increased endothelial nitric oxide synthase (eNOS) activation. Here, we evaluated the role of the β3AR-eNOS pathway and NOS isoforms in exercise-induced cardioprotection of C57Bl6 mice fed with high fat and sucrose diet (HFS) for 12 weeks and subjected or not to exercise training during the last 4 weeks (HFS-Ex).
View Article and Find Full Text PDFWe investigated the role of inducible nitric oxide (NO) synthase (iNOS) on ischemic myocardial damage in rats exposed to daily low nontoxic levels of carbon monoxide (CO). CO is a ubiquitous environmental pollutant that impacts on mortality and morbidity from cardiovascular diseases. We have previously shown that CO exposure aggravates myocardial ischemia-reperfusion (I/R) injury partly because of increased oxidative stress.
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