Abstract
Pseudoexfoliation syndrome (PES) is a microfibrillopathy and a multisystem disorder that affects the anterior segment of the eye and body tissues. The etiopathogenesis of this disorder is poorly understood; however, several theoretical mechanisms have been elucidated. These include the role of genetics, commonly involving lysyl oxidase-like 1 (LOXL1) gene on chromosome 15, vascular dysfunction caused by oxidative stress, and growth factors that induce the development of excessive fibrous connective tissue (fibrosis). The production of components of extracellular matrix found in exfoliative material is influenced by growth factors such as transforming growth factor β (TGFβ) isoforms, connective tissue growth factor, basic fibroblast growth factor, hepatocyte growth factor, and vascular endothelial growth factor. The association of clusterin with TGFβ1, role of oxidative stress, and elastosis has also been identified. Clusterin has been identified as one of the most prevalent proteins found in exfoliation deposits. Oxidative stress has been shown to induce fibrogenic responses involved in the pathogenesis of fibrotic disorders, leading to increased expression of PES-associated proteins. Ultrastructural evidence shows that PES is a kind of elastosis, characterized by the increased synthesis and accumulation of elastic microfibrils in the affected tissues in the eye.
Published Version
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