Diet induced insulin resistance is due to induction of PTEN expression.

Type 2 Diabetes (T2D) is a condition that is often associated with obesity and defined by reduced sensitivity of PI3K signaling to insulin (insulin resistance), hyperinsulinemia and hyperglycemia. Molecular causes and early signaling events underlying insulin resistance are not well understood. Insulin activation of PI3K signaling causes mTOR dependent induction of PTEN translation, a negative regulator of PI3K signaling.

IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis: A New Pathway in Chronic Kidney Disease?

Chronic kidney disease (CKD), secondary to renal fibrogenesis, is a public health burden. The activation of interstitial myofibroblasts and excessive production of extracellular matrix (ECM) proteins are major events leading to end-stage kidney disease. Recently, interleukin-15 (IL-15) has been implicated in fibrosis protection in several organs, with little evidence in the kidney.

Roles of tetraspanins during trophoblast development: bioinformatics and new perspectives.

Tetraspanins are a superfamily of membrane proteins found in all eukaryotic organisms. They act as scaffold molecules that regulate the traffic and function of other membrane/signaling proteins, resulting in important downstream cellular consequences. The aim of this work was to use transcriptomes and bioinformatics analysis to identify the tetraspanins (and their partners) involved in trophoblast differentiation.

Idiopathic nephrotic syndrome and serum permeability factors: a molecular jigsaw puzzle.

Nephrotic syndrome is traditionally defined using the triad of edema, hypoalbuminemia, and proteinuria, but this syndrome is very heterogeneous and difficult to clarify. Its idiopathic form (INS) is probably the most harmful and essentially comprises two entities: minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS). We will consider some hypotheses regarding the mechanisms underlying INS: (i) the presence of several glomerular permeability factors in the sera of patients that alter the morphology and function of podocytes leading to proteinuria, (ii) the putative role of immune cells.