Heme Oxygenase and the KidneyHeme oxygenases (HOs) are the enzymes responsible for the breakdown of heme and the generation of biliverdin/bilirubin and carbon monoxide (CO). The kidney is a complex organ consisting of many different cell types all working together for the single purpose of filtering the blood to eliminate waste products and conserving ions, minerals, and water necessary for life. HO enzymes and their products play a critical role in the normal function of the kidney as well as protecting the kidney from various insults including ischemia and exposure to nephrotoxins. For example, the HO metabolite, bilirubin, is a potent antioxidant which can limit damage to renal tubular epithelial cells following exposure to nephrotoxins associated with chemotherapy or traumatic injury. Another HO metabolite, CO, is an important vasodilator of renal blood vessels and helps protect against severe decreases in renal blood flow in conditions as diverse as exposure to radiocontrast agents and in hypertension-induced kidney disease. HO and its metabolites also play an important role in the survival of kidney cells after acute and chronic injuries by regulating important cell growth and programmed cell death pathways. The intent of this volume is to highlight the important role that HO enzymes and their related metabolites, bilirubin and CO, play in the regulation of renal function and in the response of the kidney to both acute and chronic pathologies. Table of Contents: Introduction to the HO System / HO and Renal Vascular Function / HO and Renal Tubule Function / HO and Acute Kidney Injury / HO and Chronic Kidney Injury / Future of Renal HO Research / References |
Contents
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31 HO AND PROXIMAL TUBULE FUNCTION | 15 |
33 HO AND DISTAL TUBULE FUNCTION | 18 |
HO and Acute Kidney Injury | 21 |
HO and Chronic Kidney Injury | 29 |
Future of Renal HO Research | 41 |
References | 51 |
Author Biography | 71 |
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Common terms and phrases
Abraham activity acute kidney injury afferent allograft allograft survival angiotensin antioxidant apoptosis arterial attenuates basal conditions bilirubin bilirubin levels biliverdin reductase Biol Chem blood pressure carbon monoxide cell types cellular cGMP chronic cisplatin CORMs Cre recombinase CrMP decrease demonstrated diabetic nephropathy donor effect endothelial enzyme expression ferritin Figure glomerular heme oxygenase heme oxygenase-1 hemin HO-1 gene HO-1 induction HO-1 knockout HO-2 isoform hypertension hypoxia increases in renal Induction of heme induction of HO-1 inflammation infusion inhibition inhibitors ischemia isoform Kidney Int knockout mice mediated metabolites mouse Nasjletti nitric oxide oxidase oxidative stress Panel Physiol Renal Physiol plasma bilirubin protecting the kidney protein proximal tubule reactive oxygen species renal blood flow renal cancer renal function renal medullary renal perfusion pressure renal transplantation renal tubular renal vasculature Reproduced with permission role siRNA Soc Nephrol sodium reabsorption specific Stec studies superoxide thick ascending tubule cells tumor vasoconstriction vivo Wang