Sirtuin 1 activator alleviated lethal inflammatory injury promotion of autophagic degradation of pyruvate kinase M2.

Upregulation of pyruvate kinase M2 (PKM2) is critical for the orchestration of metabolism and inflammation in critical illness, while autophagic degradation is a recently revealed mechanism that counter-regulates PKM2. Accumulating evidence suggests that sirtuin 1 (SIRT1) function as a crucial regulator in autophagy. The present study investigated whether SIRT1 activator would downregulate PKM2 in lethal endotoxemia promotion of its autophagic degradation.

REV-ERBα Agonist GSK4112 attenuates Fas-induced Acute Hepatic Damage in Mice.

Fas-induced apoptosis is a central mechanism of hepatocyte damage during acute and chronic hepatic disorders. Increasing evidence suggests that circadian clock plays critical roles in the regulation of cell fates. In the present study, the potential significance of REV-ERBα, a core ingredient of circadian clock, in Fas-induced acute liver injury has been investigated.

A disposable and sensitive non-enzymatic glucose sensor based on 3D graphene/CuO modified carbon paper electrode.

Herein, a three-dimensional graphene wall (GWs) and nano-CuO modified carbon fiber paper (CFP) electrode were used to develop a disposable and sensitive non-enzymatic glucose sensor. This sensing interface of GWs/CuO consists of an interlaced CFP on which intercrossed graphene walls (GWs) were vertically tethered in situ by radio frequency plasma enhanced chemical vapor deposition (RF-PECVD), and CuO nanoparticles (NPs) were evenly grew on the 3D GWs layer and skeleton through the complete thermal decomposition of copper acetate (Cu (CHCOO)) at high temperature. The CFP/GWs/CuO shows a large specific surface area and rich solution diffusion channels, which can expose more catalytic active sites without Nafion fixation film, thus greatly improving the electrocatalytic performance of this glucose sensor.

Diversity in mitochondrial function explains differences in vascular oxygen sensing.

Renal arteries (RAs) dilate in response to hypoxia, whereas the pulmonary arteries (PAs) constrict. In the PA, O2 tension is detected by an unidentified redox sensor, which controls K+ channel function and thus smooth muscle cell (SMC) membrane potential and cytosolic calcium. Mitochondria are important regulators of cellular redox status and are candidate vascular O2 sensors.