TGF beta and fibrosis-ironing out the wrinkles

The fibrotic disorder Posterior Capsule Opacification (PCO) is the leading secondary ocular complication following cataract surgery. PCO causes a significant loss of vision for approximately 10–30% of patients, 2–5 years post cataract removal. The formation of PCO requires additional surgical treatment, presenting an additional and substantial burden on health care providers and affects the overall well-being of cataract patients. Fibrotic disorders affect many organs of the body and are associated with hyperproliferation, cell transdifferentiation, matrix modification and contraction. Identifying the major control of these features is essential to our understanding of PCO development. Transforming growth factor beta (TGFβ) has long been implicated in fibrotic disorders and is commonly defined as the “master switch” of fibrosis. However the actions governed by TGFβ can be complex and diverse involving multiple signalling pathways and cross-talk between many signalling cascades. Significant understanding of the key pathways regulating TGFβ induced modifications in PCO has been identified using human cell and tissue culture models. These important findings and how they may be used as therapeutic targets will be presented.