Advanced glycosylation end products up-regulate connective tissue growth factor (insulin-like growth factor-binding protein-related protein 2) in human fibroblasts: a potential mechanism for expansion of extracellular matrix in diabetes mellitus.

@article{Twigg2001AdvancedGE,
  title={Advanced glycosylation end products up-regulate connective tissue growth factor (insulin-like growth factor-binding protein-related protein 2) in human fibroblasts: a potential mechanism for expansion of extracellular matrix in diabetes mellitus.},
  author={Stephen Morris Twigg and M M Chen and Alison H. Joly and S D Chakrapani and Junko Tsubaki and H S Kim and Youngman Oh and Ron G. Rosenfeld},
  journal={Endocrinology},
  year={2001},
  volume={142 5},
  pages={
          1760-9
        }
}
Expansion of extracellular matrix with fibrosis occurs in many tissues as part of the end-organ complications in diabetes, and advanced glycosylation end products (AGE) are implicated as one causative factor in diabetic tissue fibrosis. Connective tissue growth factor (CTGF), also known as insulin-like growth factor-binding protein-related protein-2 (IGFBP-rP2), is a potent inducer of extracellular matrix synthesis and angiogenesis and is increased in tissues from rodent models of diabetes. The… 
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Connective tissue growth factor/IGF-binding protein-related protein-2 is a mediator in the induction of fibronectin by advanced glycosylation end-products in human dermal fibroblasts.
TLDR
The induction of FN by AGE is partly mediated by the AGE-induced up-regulation of cell-derived CTGF and is dependent on PKC activity, which has potential implications for the expansion of extracellular matrix in diabetes mellitus by advanced glycosylation end products.
Connective tissue growth factor plays an important role in advanced glycation end product-induced tubular epithelial-to-mesenchymal transition: implications for diabetic renal disease.
TLDR
Findings suggest that CTGF represents an important independent mediator of tubular EMT, downstream of the actions of AGE or TGF-beta1, and strengthens the rationale to consider CTGF as a potential target for the treatment of diabetic nephropathy.
The up-regulation of angiotensin II receptor type 1 and connective tissue growth factor are involved in high-glucose-induced fibronectin production by cultured human dermal fibroblasts.
CCN-2 is up-regulated by and mediates effects of matrix bound advanced glycated end-products in human renal mesangial cells
TLDR
CCN-2 is induced by non-enzymatically glycated matrix and it mediates downstream fibronectin and TIMP-1 increases, thus through this mechanism potentially contributing to ECM accumulation in the renal glomerulus in diabetes.
Connective tissue growth factor and igf-I are produced by human renal fibroblasts and cooperate in the induction of collagen production by high glucose.
TLDR
It is demonstrated that both CTGF and IGF-I expressions were increased in renal fibroblasts under hyperglycemic conditions, also in the absence of TGF-beta signaling, and the cooperation between CTGF-I might be involved in glucose-induced matrix accumulation in tubulointerstitial fibrosis and might contribute to the pathogenesis of diabetic nephropathy.
Connective tissue growth factor mediates high glucose effects on matrix degradation through tissue inhibitor of matrix metalloproteinase type 1: implications for diabetic nephropathy.
TLDR
Intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy.
Glomerular expression of thrombospondin-1, transforming growth factor beta and connective tissue growth factor at different stages of diabetic nephropathy and their interdependent roles in mesangial response to diabetic stimuli
TLDR
Increased glomerular expression of all three factors occurs from the earliest stage of diabetic nephropathy, and CTGF is required for mesangial synthesis of fibronectin stimulated by high glucose or glycated albumin, and is thus a potential therapeutic target.
Secretion of collagen type IV by human renal fibroblasts is increased by high glucose via a TGF-beta-independent pathway.
TLDR
Renal fibroblasts secrete collagen type IV, which can be increased by high glucose independent of endogenous TGF-beta, which suggests that as well as the increased expression of interstitial components, renal fibroBLasts can contribute to the increase expression of the basement membrane component collagen typeIV in tubulointerstitial fibrosis observed during diabetic nephropathy.
Renal connective tissue growth factor induction in experimental diabetes is prevented by aminoguanidine.
TLDR
It is postulated that the antifibrotic effects of AG in this animal model may be partially mediated by CTGF, based on the in vitro findings in mesangial cells linking AGEs to CTGF expression.
Role of Connective Tissue Growth Factor in Mediating Hypertrophy of Human Proximal Tubular Cells Induced by Angiotensin II
TLDR
The data are the first to clearly demonstrate that CTGF might be an important mediator of Ang II-induced renal hypertrophy, which suggests that inhibiting the production of CTGF may be the new strategy in early prevention of renal fibrosis.
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References

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TLDR
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TLDR
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TLDR
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TLDR
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Connective tissue growth factor (CTGF) is a mitogenic and chemotactic factor for cultured fibroblasts that has been implicated in wound healing, fibrotic disorders and uterine function. Although the…
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TLDR
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TLDR
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Accumulation of mesangial matrix is a pivotal event in the pathophysiology of diabetic nephropathy. The molecular triggers for matrix production are still being defined. Here, suppression subtractive…
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TLDR
The results indicate that CTGF may be a common growth factor involved in renal fibrosis, and an increase in the number of cells expressing CTGF mRNA was observed at sites of chronic tubulointerstitial damage, which correlated with the degree of damage.
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