Molecular Mechanisms of Acute Renal Failure following Ischemia/Reperfusion
| Autor: | René J. P. Musters, Amanda M. G. Versteilen, Jan R. Leemreis, Pieter Sipkema, F Di Maggio, A B J Groeneveld |
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| Rok vydání: | 2004 |
| Předmět: |
0301 basic medicine
Resuscitation medicine.medical_specialty Programmed cell death Necrosis Neutrophils medicine.medical_treatment 030232 urology & nephrology Biomedical Engineering Ischemia Medicine (miscellaneous) Apoptosis Bioengineering Kidney Bioinformatics Biomaterials 03 medical and health sciences 0302 clinical medicine medicine Animals Humans Renal replacement therapy Intensive care medicine Cell damage Cytoskeleton Acute tubular necrosis Tumor Necrosis Factor-alpha business.industry General Medicine Acute Kidney Injury medicine.disease Actins Kidney Tubules 030104 developmental biology medicine.anatomical_structure Reperfusion Injury Endothelium Vascular medicine.symptom Reactive Oxygen Species business Glomerular Filtration Rate |
| Zdroj: | The International Journal of Artificial Organs. 27:1019-1029 |
| ISSN: | 1724-6040 0391-3988 |
| DOI: | 10.1177/039139880402701203 |
| Popis: | Acute renal failure (ARF) necessitating renal replacement therapy is a common problem associated with high morbidity and mortality in the critically ill. Hypotension, followed by resuscitation, is the most common etiologic factor, mimicked by ischemia/reperfusion (I/R) in animal models. Although knowledge of the pathophysiology of ARF in the course of this condition is increasingly detailed, the intracellular and molecular mechanisms leading to ARF are still incompletely understood. This review aims at describing the role of cellular events and signals, including collapse of the cytoskeleton, mitochondrial and nuclear changes, in mediating cell dysfunction, programmed cell death (apoptosis), necrosis and others. Insight into the molecular pathways in the various elements of the kidney, such as vascular endothelium and smooth muscle and tubular epithelium leading to cell damage upon I/R will, hopefully, open new therapeutic modalities, to mitigate the development of ARF after hypotensive episodes and to promote repair and resumption of renal function once ARF has developed. |
| Databáze: | OpenAIRE |
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