We recently found dysregulation of mitochondrial dynamics caused by increased Drp1 expression and cellular apoptosis of the heart in an experimental AKI animal model of renal ischemia-reperfusion.
In this regard, a better diagnostic markers to serve for this purpose are creatinine clearance, fractional excretion of magnesium (FE Mg), cystatin C. Recently, renal microvascular disease and renal ischemia have been demonstrated to correlate indirectly with the development of diabetic kidney disease and its function.
Renal mRNA expressions of megalin and cubilin, which are expressed at renal proximal tubules and uptake NGAL, decreased in animals with renal ischaemia for more than 20 minutes.
Here, pronounced increases of stromal cell-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) were substantiated in I/R kidneys from C57BL/6 mice subjected to clamp the bilateral renal pedicles to mimic renal ischemia.
ITF 1697 prevented a systemic response to IRI: a significant surge in the levels of eotaxin and IL-8 (KC; both components of WPB), IL-1α, IL-1β, and RANTES was all prevented or blunted by the administration of ITF 1697, whereas the levels of an anti-inflammatory, IL-10, and macrophage inflammatory protein-1α were upregulated in ITF 1697-treated animals.
We recently found dysregulation of mitochondrial dynamics caused by increased Drp1 expression and cellular apoptosis of the heart in an experimental AKI animal model of renal ischemia-reperfusion.
We recently found dysregulation of mitochondrial dynamics caused by increased Drp1 expression and cellular apoptosis of the heart in an experimental AKI animal model of renal ischemia-reperfusion.
Administration of DNase I, which degrades neutrophil extracellular traps or the PAD-specific inhibitor YW3-56 before ischemia, partially prevented renal ischemia/reperfusion-induced AKI.
We recently found dysregulation of mitochondrial dynamics caused by increased Drp1 expression and cellular apoptosis of the heart in an experimental AKI animal model of renal ischemia-reperfusion.
In vivo experiments in rats revealed that Egr-1 protein increases, whereas 11beta-HSD2 mRNA decreases, in kidney tissue after unilateral renal ischemia and in humans the renal activity of 11beta-HSD2 as assessed by the urinary ratio of (tetrahydrocortisol+5alpha-tetrahydrocortisol)/tetrahydrocortisone declined when volunteers were exposed to hypoxemia at high altitude up to 7000 m. Thus, hypoxia decreases 11beta-HSD2 transcription and activity by inducing Egr-1 in vivo and in vitro.
Nanoparticle-mediated dual delivery of resveratrol and DAP5 ameliorates kidney ischemia/reperfusion injury by inhibiting cell apoptosis and inflammation.
Lipopolysaccharide-induced cross-tolerance against renal ischemia-reperfusion injury is mediated by hypoxia-inducible factor-2α-regulated nitric oxide production.
We postulate that chronic intermittent hypotension and renal ischemia may lead to erythropoietin secretion, and this cascade could represent a newly recognized cause of secondary erythrocytosis.
Rats were randomly assigned to four experimental groups following median laparotomy and right nephrectomy: Sham (n = 6); 30-min left renal ischemia (RI) only (n = 20); RI + rIC (n = 20) (four 5-min cycles of limb ischemia interspersed with 5-min limb reperfusion during RI); and RI + erythropoietin pretreatment (EPO) (n = 20).
In this study, we show that both mRNA and protein levels of Foxc2 increase 1 day after kidney ischemia/reperfusion in sublethally injured tubular cells and that the protein is located in the cytoplasm rather than the nucleus of these cells. in vitro studies of cultured tubular cells confirm the cytoplasmic location of Foxc2 and show that increased cytoplasmic expression of Foxc2 correlates with epithelial differentiation rather than dedifferentiation.
Activin A modulated growth of BrdU/Pax-2 double-positive cells since an administration of follistatin increased; conversely, exogenous activin A decreased the number of BrdU/Pax-2 double-positive cells after renal ischemia.