AI Article Synopsis

  • CTGF is an important signaling molecule involved in various physiological processes and is often upregulated in fibrotic diseases related to ECM remodeling.
  • It interacts with TGF-β through both SMAD-dependent and independent pathways, indicating that targeting CTGF could reduce potential side effects linked to TGF-β's broader functions.
  • Elevated CTGF and TGF-β levels contribute to glaucoma through increased intraocular pressure due to excessive ECM buildup, positioning CTGF as a promising therapeutic target for managing this eye condition.

Article Abstract

Connective tissue growth factor (CTGF) is a distinct signaling molecule modulating many physiological and pathophysiological processes. This protein is upregulated in numerous fibrotic diseases that involve extracellular matrix (ECM) remodeling. It mediates the downstream effects of transforming growth factor beta (TGF-β) and is regulated via TGF-β SMAD-dependent and SMAD-independent signaling routes. Targeting CTGF instead of its upstream regulator TGF-β avoids the consequences of interfering with the pleotropic effects of TGF-β. Both CTGF and its upstream mediator, TGF-β, have been linked with the pathophysiology of glaucomatous optic neuropathy due to their involvement in the regulation of ECM homeostasis. The excessive expression of these growth factors is associated with glaucoma pathogenesis via elevation of the intraocular pressure (IOP), the most important risk factor for glaucoma. The raised in the IOP is due to dysregulation of ECM turnover resulting in excessive ECM deposition at the site of aqueous humor outflow. It is therefore believed that CTGF could be a potential therapeutic target in glaucoma therapy. This review highlights the CTGF biology and structure, its regulation and signaling, its association with the pathophysiology of glaucoma, and its potential role as a therapeutic target in glaucoma management.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10657592PMC
http://dx.doi.org/10.1177/15353702231199466DOI Listing

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