Markus Bleich

TL;DR: It is demonstrated that renal tubules do not undergo sensitization to necroptosis upon genetic ablation of either FADD or caspase-8 and that the RIPK1 inhibitor necrostatin-1 (Nec-1) does not protect freshly isolated tubules from hypoxic injury, and ferroptosis mediates postischemic and toxic renal necrosis.

TL;DR: This paper attempts to summarize some ontogenetic and lifestyle traits that lead to an increased tolerance towards high environmental pCO2, and suggests that compensation of extracellular acid-base status in turn may be important in avoiding metabolic depression.

TL;DR: It is shown that the novel β-subunit KCNE3 markedly changes KCNQ1 properties to yield currents that are nearly instantaneous and depend linearly on voltage, which indicates that these proteins may assemble to form the potassium channel that is important for cyclic AMP-stimulated intestinal chloride secretion and that is involved in secretory diarrhoea and cystic fibrosis.

TL;DR: The present data indicate that MR-deficient neonates die because they are not able to compensate renal Na+ loss and MR knockout mice will be a suitable tool for the search of these genes.

TL;DR: The identification of a specific NF-κB promoter module activated in the inflammatory stress response of progressive DN has helped to characterize upstream pathways as potential targets for the treatment of progressive renal diseases such as DN.