Research progress on mechanism of action of early prediction in acute kidney injury by tissue inhibitor of metalloproteinase 2 and insulin-like growth factor binding protein 7
Severe infections,ischemia and hypoxia can lead to acute kidney injury,causing damage to renal blood vessels,increased release of inflammatory cells and pro-inflammatory cytokines in renal tubules,and triggering and upregulation of glycolysis processes.Increase of inflammatory cells and vascular damage lead to decrease in the expression of small molecule ribonucleotides,thereby upregulating matrix metalloproteinases in tubular epithelial cells.Tissue inhibitor of metalloproteinase 2(TIMP-2)can widely inhibit activity of matrix metalloproteinases(priority binding to matrix metalloproteinase 2),in order to restore dynamic balance between the two,expression of TIMP-2 increased,simultaneously,pro-inflammatory cytokines can directly induce secretion of TIMP-2 by tubular epithelial cells.Transforming growth factorβ1 is involved in increase of insulin-like growth factor binding protein 7(IGFBP-7)during acute kidney injury.IGFBP-7 can prolong half-life of insulin and insulin-like growth factor 1,promote their binding to receptors,prolong activation of related pathways,and catalyze tyrosine protein kinase activity,leading to increased activity of phosphofructokinase and ultimately causing activation and increased flux of glycolysis in acute renal injury renal tubular epithelial cells.TIMP-2 and IGFBP-7 can aggravate cell cvcle arrest and can be used as markers of cell cvcle arrest in acute kidnev iniurv.
Acute kidney injuryMarkersMatrix metalloproteinaseTissue inhibitor of metalloproteinase 2Insulin-like growth factor binding protein 7
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