Tuanjie Chang

TL;DR: Endogenously produced H2S protects against the development of hyperglycemia-induced endothelial dysfunction ex vivo, and it is hypothesized that, in hyperglycemic endothelial cells, mitochondrial ROS production and increased H1N1 catabolism form a positive feed-forward cycle.

TL;DR: These findings provide the first evidence that low levels of H(2)S decrease reactive oxygen species and improve cell viability and by doing so limit cellular damage induced by HCY.

TL;DR: In conclusion, MG induces significant generation of NO and O2*- in rat VSMCs, which in turn causes ONOO- formation and the consequential ROS/RNS generation would alter cellular signaling pathways, contributing to the development of different insulin resistance states such as diabetes or hypertension.

TL;DR: Investigation in spontaneously hypertensive rats found increased aortic MG, AGE formation and oxidative stress were associated with blood pressure increase in SHR, which may cause endothelial dysfunction and altered vascular reactivity.

TL;DR: Increased methylglyoxal, AGEs, oxidative stress and reduced eNOS along with structural remodeling of the vessel wall in the aorta and mesenteric artery likely play a role in the pathogenesis of hypertension.