Regulators of vascular permeability: potential sites for intervention in the treatment of macular edema

Doc Ophthalmol. 1999;97(3-4):251-60. doi: 10.1023/a:1002196930726.


Rather than being a non-specific reaction to a noxious stimulus, breakdown of the capillary blood-retinal barrier causing macular edema appears to be dependent on a number of active processes which may be open to pharmacological manipulation. Extracellular influences which may affect barrier function include serum and neighboring cell types, which act though cytokines, such as vascular endothelial growth factor and transforming growth factor-beta, and other factors. A number of intracellular pathways acting on the cytoskeleton and components of the intercellular junctional complexes have been identified which mediate agonist-induced leak of the vascular endothelium. The further elucidation of these processes may be useful in the development of better treatments for breakdown of the inner blood-retinal barrier.

Publication types

  • Review

MeSH terms

  • Animals
  • Blood-Retinal Barrier*
  • Capillary Permeability* / drug effects
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism
  • Humans
  • Macular Edema / drug therapy*
  • Macular Edema / metabolism
  • Macular Edema / pathology
  • Phosphorylation
  • Protein Kinase C / metabolism
  • Signal Transduction
  • Tyrosine / metabolism


  • Tyrosine
  • Protein Kinase C