Coenzyme-A-Responsive Nanogel-Coated Electrochemical Sensor for Osteoarthritis-Detection-Based Genetic Models.

An electrochemical sensor sensitive to coenzyme A (CoA) was designed using a CoA-responsive polyallylamine-manganese oxide-polymer dot nanogel coated on the electrode surface to detect various genetic models of osteoarthritis (OA). The CoA-responsive nanogel sensor responded to the abundance of CoA in OA, causing the breakage of MnO in the nanogel, thereby changing the electroconductivity and fluorescence of the sensor. The CoA-responsive nanogel sensor was capable of detecting CoA depending on the treatment time and distinguishing the response towards different OA genetic models that contained different levels of CoA (wild type/WT, NudT7 knockout/N7KO, and Acot12 knockout/A12KO).

Electrochemical and Fluorescence MnO-Polymer Dot Electrode Sensor for Osteoarthritis-Based Peroxisomal β-Oxidation Knockout Model.

A coenzyme A (CoA-SH)-responsive dual electrochemical and fluorescence-based sensor was designed utilizing an MnO-immobilized-polymer-dot (MnO@D-PD)-coated electrode for the sensitive detection of osteoarthritis (OA) in a peroxisomal β-oxidation knockout model. The CoA-SH-responsive MnO@D-PD-coated electrode interacted sensitively with CoA-SH in OA chondrocytes, triggering electroconductivity and fluorescence changes due to cleavage of the MnO nanosheet on the electrode. The MnO@D-PD-coated electrode can detect CoA-SH in immature articular chondrocyte primary cells, as indicated by the significant increase in resistance in the control medium (R = 2.

Pan-Src kinase inhibitor treatment attenuates diabetic kidney injury via inhibition of Fyn kinase-mediated endoplasmic reticulum stress.

Src family kinases (SFKs) have been implicated in the pathogenesis of kidney fibrosis. However, the specific mechanism by which SFKs contribute to the progression of diabetic kidney disease (DKD) remains unclear. Our preliminary transcriptome analysis suggested that SFK expression was increased in diabetic kidneys and that the expression of Fyn (a member of the SFKs), along with genes related to unfolded protein responses from the endoplasmic reticulum (ER) stress signaling pathway, was upregulated in the tubules of human diabetic kidneys.

Peroxisomal Fitness: A Potential Protective Mechanism of Fenofibrate against High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice.

Background: Non-alcoholic fatty liver disease (NAFLD) has been increasing in association with the epidemic of obesity and diabetes. Peroxisomes are single membrane-enclosed organelles that play a role in the metabolism of lipid and reactive oxygen species. The present study examined the role of peroxisomes in high-fat diet (HFD)-induced NAFLD using fenofibrate, a peroxisome proliferator-activated receptor α (PPARα) agonist.

Associations of Circulating Irisin with FNDC5 Expression in Fat and Muscle in Type 1 and Type 2 Diabetic Mice.

Irisin is an exercise-induced myokine, suggested to exert beneficial effects on metabolism. However, the studies on the regulation of irisin secretion and the expression of its precursor FNDC5 have shown conflicting data. The discrepancies among previous correlation studies in humans are related to the heterogeneity of the study population.

Dojuksan ameliorates tubulointerstitial fibrosis through irisin-mediated muscle-kidney crosstalk.

Background: Sarcopenia progresses in chronic kidney disease (CKD) and is positively correlated with mortality in end-stage kidney disease patients. Circulating irisin, an exercise-induced myokine, gradually decreases during CKD stage progression. Irisin inhibits the progression of kidney fibrosis, which is the final common outcome of CKD.

Cigarette smoke inhalation aggravates diabetic kidney injury in rats.

Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease. Epidemiological studies have demonstrated that cigarette smoke or nicotine is a risk factor for the progression of chronic kidney injury. The present study analyzed the kidney toxicity of cigarette smoke in experimental rats with DKD.

Impaired Peroxisomal Fitness in Obese Mice, a Vicious Cycle Exacerbating Adipocyte Dysfunction Oxidative Stress.

Peroxisome is a critical organelle for fatty acid oxidation (FAO) and metabolism of reactive oxygen species (ROS). Increased oxidative stress in adipose tissue contributes to the development of insulin resistance and metabolic syndrome in obesity. This study aimed to investigate the role of peroxisomal fitness in maintaining adipocyte function, which has been under-rated in the obesity research area.

Peroxiredoxin 3 deficiency accelerates chronic kidney injury in mice through interactions between macrophages and tubular epithelial cells.

Chronic kidney disease (CKD) has become epidemic worldwide. Mitochondrial reactive oxygen species (ROS)-induced oxidative stress is an important mediator of CKD, and Prx3 plays a critical role in maintenance of mitochondrial ROS. The present study examined the role of Prx3 in the context of fibrosis, a common feature of CKD, using Prx3 KO mice under obstructive and diabetic stress.

A novel pan-Nox inhibitor, APX-115, protects kidney injury in streptozotocin-induced diabetic mice: possible role of peroxisomal and mitochondrial biogenesis.

NADPH oxidase (Nox)-derived reactive oxygen species (ROS) are increasingly recognized as a key factor in inflammation and extracellular matrix accumulation in diabetic kidney disease. APX-115 (3-phenyl-1-(pyridin-2-yl)-4-propyl-1-5-hydroxypyrazol HCl) is a novel orally active pan-Nox inhibitor. The objective of this study was to compare the protective effect of APX-115 with a renin-angiotensin system inhibitor (losartan), the standard treatment against kidney injury in diabetic patients, on streptozotocin (STZ)-induced diabetic kidney injury.