Excessive deposition of extracellular matrix (ECM) in the kidney is the hallmark of @entity2316 . Although the amount of ECM deposited in the kidney depends on the balance between the synthesis and degradation of ECM, the role of ECM degradation in matrix remodeling has been less well appreciated. High @entity413 , advanced glycation end products, @entity2178 , and @entity2533 all increase intracellular reactive @entity26 species (ROS) in renal cells and contribute to the development and progression of @entity2316 . The role of ROS in increased ECM synthesis has been well documented. ROS may also play a critical role in decreased ECM degradation by mediating high @entity413 - and @entity2533 -induced inhibition of the proteolytic system, plasmin, and matrix metalloproteinases in the glomeruli. A recent observation suggests that ROS play an important role in tubulointerstitial @entity82 by mediating @entity2533 -induced epithelial-mesenchymal transition (EMT). Accelerated ECM degradation is required to disrupt tubular basement membrane and complete EMT. ROS thus seem to be involved in both decreased and increased ECM degradation. It is not clear how cells determine when and where to increase or decrease ECM degradation in response to ROS. Precise definition of ROS-activated signaling pathways leading to ECM remodeling in the kidney will provide new strategies to prevent or treat @entity2316 .

Reactive XXXX species and matrix remodeling in diabetic kidney.

@entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity2316 :: ('MESH:D003928', 'Disease') :: ['diabetic nephropathy', 'diabetic renal injury'] @entity2178 :: ('183', 'Gene') :: ['angiotensin II'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity2533 :: ('7040', 'Gene') :: ['TGF-beta1'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity26 :: (MESH:D010100,Chemical) :: ['oxygen']
