The kidney expression of matrix metalloproteinase-9 in the diabetic nephropathy of Kkay mice

Guo, Qinghua; Lu, Juming; Pan, Changyu; Zhang, Lu; Zou, Xiaoshuang; Mu, Yiming

doi:10.1016/j.jdiacomp.2007.10.002

Cited by 24 publications

(16 citation statements)

References 12 publications

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“…13,16 Gelatinases MMP2 and -9 can be activated by membrane type 1 MMP, also known as MMP14. We and others have shown that diabetic conditions induce upregulation of endothelial MMP9, 16 MMP2, 29 and urinary MMP14 31 ; their enzymatic activities are elevated in diabetic human 31,32 and mouse 33 kidneys. The dysregulation of MMP2 and -9 activities has been associated in the pathophysiology of several diabetic comorbidities.…”

mentioning

confidence: 72%

Blocking matrix metalloproteinase-mediated syndecan-4 shedding restores the endothelial glycocalyx and glomerular filtration barrier function in early diabetic kidney disease

Ramnath

Butler

Newman

et al. 2020

Kidney International

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mentioning

confidence: 72%

Blocking matrix metalloproteinase-mediated syndecan-4 shedding restores the endothelial glycocalyx and glomerular filtration barrier function in early diabetic kidney disease

Ramnath

Butler

Newman

et al. 2020

Kidney International

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“…In addition, it is also reported that Simvastatin protects kidney damage of diabetic rat through the suppression of MMP9 expression [147]. Along these lines, the expression of MMP9 mRNA and protein were found to be up-regulated compared with the control group in 16 weeks of Kkay mice with glomerular sclerosing lesions [148]. Similarly, Szu li et al reported reduced glomerular hyperfiltration and glomerular basement membrane thickening in diabetic MMP9 −/− mice than diabetic WT mice [138].…”

Section: Mmps and Diabetic Nephropathymentioning

confidence: 99%

A Glimpse of Matrix Metalloproteinases in Diabetic Nephropathy

Xiao

et al. 2014

CMC

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Matrix metalloproteinases (MMPs) are proteolytic enzymes belonging to the family of zinc-dependent endopeptidases that are capable of degrading almost all the proteinaceous components of the extracellular matrix (ECM). It is known that MMPs play a role in a number of renal diseases, such as, various forms of glomerulonephritis and tubular diseases, including some of the inherited kidney diseases. In this regard, ECM accumulation is considered to be a hallmark morphologic finding of diabetic nephropathy, which not only is related to the excessive synthesis of matrix proteins, but also to their decreased degradation by the MMPs. In recent years, increasing evidence suggest that there is a good correlation between the activity or expression of MMPs and progression of renal disease in patients with diabetic nephropathy in humans and in various experimental animal models. In such a diabetic milieu, the expression of MMPs is modulated by high glucose, advanced glycation end products (AGEs), TGF-β, reactive oxygen species (ROS), transcription factors and some of the microRNAs. In this review, we focused on the structure and functions of MMPs, and their role in the pathogenesis of diabetic nephropathy.

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“…With respect to diabetes, in the KKAy mouse (a rodent model of type 2 DM), expression of MMP-9 in the kidneys of mice that developed nephropathy was enhanced when compared to renal expression of this gelatinase in control animals [70]. In addition, increased urinary concentrations of MMP-9 have been detected in patients with type 2 DM and diabetic nephropathy, and the levels of MMP-9 increased in accordance with the degree of albuminuria (i.e., microalbuminuria < macroalbuminuria) [71, 72].…”

Section: Gelatinases (Mmp-2 and Mmp-9)mentioning

confidence: 99%

Matrix metalloproteinases: their potential role in the pathogenesis of diabetic nephropathy

Thrailkill

Bunn

Fowlkes

2008

Endocr

161

127

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Matrix metalloproteinases (MMPs), a family of proteinases including collagenases, gelatinases, stromely-sins, matrilysins, and membrane-type MMPs, affect the breakdown and turnover of extracellular matrix (ECM).Moreover, they are major physiologic determinants of ECM degradation and turnover in the glomerulus. Renal hypertrophy and abnormal ECM deposition are hallmarks of diabetic nephropathy (DN), suggesting that altered MMP expression or activation contributes to renal injury in DN. Herein, we review and summarize recent information supporting a role for MMPs in the pathogenesis of DN. Specifically, studies describing dysregulated activity of MMPs and/or their tissue inhibitors in various experimental models of diabetes, including animal models of type 1 or type 2 diabetes, clinical investigations of human type 1 or type 2 diabetes, and kidney cell culture studies are reviewed. KeywordsGelatinase; Podocyte; Extracellular matrix; Proteinases; Proteinuria Diabetic nephropathy-general overviewDiabetic nephropathy is stated to be the most common cause of end-stage renal disease in the United States [1]. Between 20% and 30% of patients with type 1 diabetes mellitus (DM) or type 2 DM will develop nephropathy [1], and among patients with type 1 DM, diabetic nephropathy develops in 40-50% of patients with a 20-year history of disease [2]. Among those individuals who develop renal dysfunction, several risk factors for the development of renal disease have been identified, including duration of diabetes, age at diagnosis, race, systemic or glomerular hypertension, poor glycemic control, genetic predisposition to kidney disease, and dietary composition [1][2][3]. However, the precise pathogenic mechanisms involved in the initiation and progression of diabetic nephropathy remain incompletely understood.The development of diabetic nephropathy has been described as a five-stage process, progressing from glomerular hyperfiltration and nephromegaly (Stage 1), to glomerular basement membrane thickening and mesangial expansion (Stage 2), to microalbuminuria and eventual decline in glomerular filtration rate (Stage 3), to frank proteinuria with severe hypertension and sequelae of moderate to severe renal insufficiency (Stage 4), to eventual endstage renal disease (Stage 5) [4,5]. It has been hypothesized that the early changes in glomerular basement membrane thickness and content ultimately affect filtration properties of the © Humana Press Inc. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript glomerular basement membrane, leading first to increased urinary albumin excretion and eventually to proteinuria. Similar histological findings are also seen in many rodent models of diabetic nephropathy. Because enlargement of the kidney mesangium due to extracellular matrix over-accumulation is a major characteristic of diabetic nephropathy, and because MMPs produced by the mesangial cell account for up to 70% of extracellular matrix degradation and turnover in the kidney during normal matrix remodeling,...

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The kidney expression of matrix metalloproteinase-9 in the diabetic nephropathy of Kkay mice

Cited by 24 publications

References 12 publications

Blocking matrix metalloproteinase-mediated syndecan-4 shedding restores the endothelial glycocalyx and glomerular filtration barrier function in early diabetic kidney disease

Blocking matrix metalloproteinase-mediated syndecan-4 shedding restores the endothelial glycocalyx and glomerular filtration barrier function in early diabetic kidney disease

A Glimpse of Matrix Metalloproteinases in Diabetic Nephropathy

Matrix metalloproteinases: their potential role in the pathogenesis of diabetic nephropathy

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