Susann Patschan

TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: R renal ischemia rapidly mobilizes EPCs, which transiently home to the spleen, acting as a temporary reservoir of mobilized E PCs, suggesting the role of the recruited EPC’s in the functional rescue.

TL;DR: To ascribe to NO deficiency in endothelial cells the function of a profibrotic stimulus associated with the expression of an antiangiogenic fragment of collagen XVIII (endostatin) is ascribed and evidence of endothelial-mesenchymal transdifferentiation in the course of inhibition of NOS by a pathophysiologically important antagonist, asymmetric dimethylarginine is provided.

TL;DR: Observations appear to represent a mechanistic molecular cascade whereby advanced glycation end products like GC induce sphingomyelinase activity, accumulation of ceramide, clustering, and later internalization of lipid rafts.

TL;DR: In this article, Uric acid (UA) is consistently overproduced by ischemic tissues and has been shown to exert immunomodulatory functions, which may serve as a universal herald of tissue injury to accelerate the recruitment of EPCs.