Wiley Interdiscip Rev Syst Biol Med - Ischemic kidney injury and mechanisms of tissue repair.

Tópicos

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{ risk(3053) factor(974) diseas(938) }
{ can(774) often(719) complex(702) }
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{ research(1218) medic(880) student(794) }
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Resumo

Acute kidney injury (AKI) may result from ischemia or by the use of nephrotoxic agents. The incidence of AKI is variable, depends on comorbidities, and ranges from 5 to 35% in all hospitalized patients. The mechanisms of kidney injury exist within a large network of signaling pathways driven by interplay of inflammatory cytokines/chemokines, reactive oxygen species (ROS), and apoptotic factors. The effects and progression of injury overlap extensively with the remarkable ability of the kidney to repair itself both by intrinsic and extrinsic mechanisms that involve specific cell receptors/ligands as well as possible paracrine influences. The fact that kidney injury is usually part of a generalized comorbid condition makes it all the more challenging in terms of assessment of severity. In this review, we attempt to analyze the mechanisms of ischemic injury and repair in acute and chronic kidney disease from the perspectives of both preclinical and human studies.

Resumo Limpo

acut kidney injuri aki may result ischemia use nephrotox agent incid aki variabl depend comorbid rang hospit patient mechan kidney injuri exist within larg network signal pathway driven interplay inflammatori cytokineschemokin reactiv oxygen speci ros apoptot factor effect progress injuri overlap extens remark abil kidney repair intrins extrins mechan involv specif cell receptorsligand well possibl paracrin influenc fact kidney injuri usual part general comorbid condit make challeng term assess sever review attempt analyz mechan ischem injuri repair acut chronic kidney diseas perspect preclin human studi

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