Abstract
Since its discovery in 1991, connective tissue growth factor (CCN2; formerly named CTGF), a member of the CCN family of genes, has been shown to have quite diverse biological functions. Our laboratory was among the first to provide evidence for a causal role for CCN2 in the pathogenesis of diabetic nephropathy (DN). We suggested its criticality as downstream profibrotic factor stimulated by both transforming growth factor (TGF)-βdependent and -independent mechanisms, and as such, a novel target for therapeutic intervention. Proof is now being provided for its role in the fibrosis and sclerosis that occurs in the glomerulus, and likely in the interstitium, in DN. This chapter will focus first on the evidence for a causal role, second on the recently discovered mechanisms and factors involved in regulation of CCN2, and third on the direction we envision the research heading, including possibilities for novel therapeutics and diagnostics targeting CCN.