Abstract
Around the world diabetic kidney disease (DKD) is the main cause of chronic kidney disease (CKD), which is characterized by mesangial expansion, glomerulosclerosis, tubular atrophy, and interstitial fibrosis. The hallmark of the pathogenesis of DKD is an increased extracellular matrix (ECM) accumulation causing thickening of the glomerular and tubular basement membranes, mesangial expansion, sclerosis, and tubulointerstitial fibrosis. The matrix metalloproteases (MMPs) family are composed of zinc-dependent enzymes involved in the degradation and hydrolysis of ECM components. Several MMPs are expressed in the kidney; nephron compartments, vasculature and connective tissue. Given their important role in DKD, several studies have been performed in patients with DKD proposing that the measurement of their activity in serum or in urine may become in the future markers of early DKD. Studies from diabetic nephropathy experimental models suggest that a balance between MMPs levels and their inhibitors is needed to maintain renal homeostasis. This review focuses in the importance of the MMPs within the kidney and their modifications at the circulation, kidney and urine in patients with DKD. We also cover the most important studies performed in experimental models of diabetes in terms of MMPs levels, renal expression and its down-regulation effect.
Highlights
Diabetic kidney disease (DKD) is the main cause of chronic kidney disease (CKD) which is characterized by mesangial expansion, glomerulosclerosis, tubular atrophy, and interstitial fibrosis
We describe the importance of the matrix metalloproteases (MMPs) family within the kidney and their modifications at the circulation, kidney and urine in patients with DKD
Taken together MMPs and tissue inhibitors of metalloproteinases (TIMPs) are involved in the development and progression of diabetic nephropathy (DN)
Summary
Diabetic kidney disease (DKD) is the main cause of chronic kidney disease (CKD) which is characterized by mesangial expansion, glomerulosclerosis, tubular atrophy, and interstitial fibrosis. The MMPs were discovered in the early 60s and are involved in the collagen degradation processes during the tadpole tail reabsorption [4] Since this family of enzymes and their roles have been expanded. MMP-2 and MMP-9, have the ability to degrade type IV collagen, the major component of the glomerular basement membrane; the interstitial collagenases, MMP-1, MMP-8 and MMP-13, hydrolyze collagen I and III Considering their important role in DKD, several studies have been performed in patients with DKD proposing that the measurement of their activity in serum or urine may become in the future markers of early DKD. We cover the most important studies performed in experimental models of diabetes in terms of MMPs levels, renal expression and its inhibition effects
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