Matrix Metalloproteinases-7 and Kidney Fibrosis

Ke, Ben; Fan, Chuqiao; Yang, Liping; Fang, Xiangdong

doi:10.3389/fphys.2017.00021

Cited by 58 publications

(81 citation statements)

References 70 publications

(90 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In experimental models of kidney fibrosis, MMP-9 is produced from mesangial, glomerular, epithelial and endothelial cells, fibroblasts and macrophages in the kidney [64]. Renal MMP-9 is at low levels in the absence of pathology while advancing age causes decreased MMP-9 and increased TIMP-1 expression, which contributes to the decline in collagen degradation [65]. MMP-9 processes a variety of ECM substrates such as collagens, elastin, fibronectin and others; non-ECM substrates and even other MMPs (MMP-2 and MMP-13) and itself.…”

Section: Clusterin (Clu)mentioning

confidence: 99%

Biomarkers in Progressive Chronic Kidney Disease. Still a Long Way to Go

Ntrinias

Papasotiriou

Balta

et al. 2019

Prilozi

View full text Add to dashboard Cite

The traditional chronic kidney disease (CKD) biomarkers (eGFR based on serum creatinine, sex and age and albuminuria) cannot predict a patient’s individual risk for developing progressive CKD. For this reason, it is necessary to identify novel CKD biomarkers that will be able to predict which patients are prone to develop progressive disease and discriminate between disease processes in different parts of the nephron (glomeruli or tubules). A good biomarker should change before or simultaneously with lesion development and its changes should correlate strongly with lesion development. Also, there should be a close relationship between severity of injury and amount of detectable biomarker and its levels should decrease with diminishing injury. Among the large number of molecules under investigation, we have reviewed the most promising ones: NGAL and KIM-1, MCP-1, MMP-9, clusterin, MMP-9, TIMP-1, Procollagen I alpha 1 and suPAR. All these, have been studied as biomarkers for prediction of CKD progression in cohorts of patients with chronic kidney disease of different stages and various aetiologies (proteinuric and non-proteinuric, glomerulonephritides, diabetic, hypertensive and polycystic kidney disease). There is evidence that these molecules could be useful as biomarkers for progressive chronic kidney disease, however, the available data are not enough to draw final conclusions. Further studies with large cohorts and long follow-up are required to identify appropriate biomarkers, that will be able to accurately and reliably define the risk for progressive chronic kidney disease.

show abstract

Section: Clusterin (Clu)mentioning

confidence: 99%

Biomarkers in Progressive Chronic Kidney Disease. Still a Long Way to Go

Ntrinias

Papasotiriou

Balta

et al. 2019

Prilozi

View full text Add to dashboard Cite

show abstract

“…13 Structurally, MMP-7 is one of the smallest MMPs, and it is synthesized as an inactive zymogen. 14…”

mentioning

confidence: 99%

Matrix metalloproteinase-7 protects against acute kidney injury by priming renal tubules for survival and regeneration

Zhou

Zhu

et al. 2019

Kidney International

View full text Add to dashboard Cite

Matrix metalloproteinase-7 (MMP-7) is a secreted endopeptidase that degrades a broad range of substrates. Recent studies have identified MMP-7 as an early biomarker to predict severe acute kidney injury (AKI) and poor outcomes after cardiac surgery; however, the role of MMP-7 in the pathogenesis of AKI is unknown. In this study, we investigated the expression of MMP-7 and the impact of MMP-7 deficiency in several models of AKI. MMP-7 was induced in renal tubules following ischemia/ reperfusion injury or cisplatin administration, and in folic acid-induced AKI. MMP-7 knockout mice experienced higher mortality, elevated serum creatinine, and more severe histologic lesions after ischemic or toxic insults. Tubular apoptosis and interstitial inflammation were more prominent in MMP-7 knockout kidneys. These histologic changes were accompanied by increased expression of FasL and other components of the extrinsic apoptotic pathway, as well as increased expression of pro-inflammatory chemokines. In a rescue experiment, exogenous MMP-7 ameliorated kidney injury in MMP-7 knockout mice after ischemia/ reperfusion. In vitro, MMP-7 protected tubular epithelial cells against apoptosis by directly degrading FasL. In isolated tubules ex vivo, MMP-7 promoted cell proliferation by degrading E-cadherin and thereby liberating b-catenin, priming renal tubules for regeneration. Taken together, these results suggest that induction of MMP-7 is protective in AKI by degrading FasL and mobilizing b-catenin, thereby priming kidney tubules for survival and regeneration.Matrix metalloproteinase-7 (MMP-7) is an early and valuable biomarker for predicting severe AKI and poor outcomes in patients after cardiac surgery. The present study indicates that induction of endogenous MMP-7 is protective in AKI by priming kidney tubules to survival and regeneration. These results suggest that other urinary biomarkers of the early phase of AKI manifest an initial attempt of the kidney to protect against injury and to promote repair after AKI. Whether infusion of exogenous MMP-7 can protect kidneys against AKI in patients warrants further investigation. www.kidney-international.org b a s i c r e s e a r c h Kidney International (2019) 95, 1167-1180

show abstract

“…Table 10). 29 Among the genes displaying the highest influence score in the network analysis based on the comparison between group 1 and 2 we found TP53 and EP300 (Fig. 4e, Suppl.…”

Section: Early Discrimination Of Kidney Disease Progressionmentioning

confidence: 89%

Transcriptional trajectories of human kidney disease progression

Cippà

Sun

Liu

et al. 2018

Preprint

View full text Add to dashboard Cite

Our molecular understanding of clinical conditions progressing from acute organ injury to irreversible dysfunction is limited. We used renal transplantation as a model to characterize the transcriptional response along the transition from acute kidney injury to allograft fibrosis in humans. The integrated analysis of 163 transcriptomes with machine learning techniques identified shared and divergent transcriptional trajectories determining distinct clinical outcomes in a heterogeneous population. The molecular map of renal responses to injury was validated in a mouse ischemia-reperfusion injury model and highlighted early markers of disease progression. This generally applicable approach opens the way for an unbiased analysis of progressive diseases.

show abstract

Matrix Metalloproteinases-7 and Kidney Fibrosis

Cited by 58 publications

References 70 publications

Biomarkers in Progressive Chronic Kidney Disease. Still a Long Way to Go

Biomarkers in Progressive Chronic Kidney Disease. Still a Long Way to Go

Matrix metalloproteinase-7 protects against acute kidney injury by priming renal tubules for survival and regeneration

Transcriptional trajectories of human kidney disease progression

Contact Info

Product

Resources

About