Abstract
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD). The development and progression of DN might involve multiple factors. Connective tissue growth factor (CCN2, originally known as CTGF) is the one which plays a pivotal role. Therefore, increasing attention is being paid to CCN2 as a potential therapeutic target for DN. Up to date, there are also many drugs or agents which have been shown for their protective effects against DN via different mechanisms. In this review, we only focus on the potential renoprotective therapeutic agents which can specifically abolish CCN2 expression or nonspecifically inhibit CCN2 expression for retarding the development and progression of DN.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anthocyanins / chemistry
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Antibodies, Monoclonal / chemistry
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Connective Tissue Growth Factor / antagonists & inhibitors*
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Connective Tissue Growth Factor / metabolism
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Diabetes Mellitus / drug therapy
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Diabetes Mellitus / metabolism*
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Diabetic Nephropathies / drug therapy
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Diabetic Nephropathies / metabolism*
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Disease Progression
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Exenatide
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Guanidines / chemistry
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Humans
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Hydroxymethylglutaryl-CoA Reductase Inhibitors / metabolism
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Inflammation
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Kidney / drug effects*
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Kidney Failure, Chronic / pathology
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Mice
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Mycophenolic Acid / analogs & derivatives
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Mycophenolic Acid / chemistry
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Oligonucleotides, Antisense / genetics
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Peptides / chemistry
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Renin-Angiotensin System
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Spironolactone / chemistry
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Venoms / chemistry
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ortho-Aminobenzoates / chemistry
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rho-Associated Kinases / metabolism
Substances
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Anthocyanins
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Antibodies, Monoclonal
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CCN2 protein, human
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CCN2 protein, mouse
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Guanidines
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Oligonucleotides, Antisense
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Peptides
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Venoms
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ortho-Aminobenzoates
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Connective Tissue Growth Factor
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Spironolactone
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Exenatide
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rho-Associated Kinases
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Mycophenolic Acid
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tranilast
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pimagedine