From: Pseudoexfoliation syndrome, a systemic disorder with ocular manifestations
Molecules related to PXS | Known function | Nature of association |
---|---|---|
Copper-dependent monoamine oxidase secreted by fibrogenic cells. Catalyzes covalent cross-linking of collagen and elastin in ECM formation | -Gene polymorphisms linked to PXS in multiple studies | |
-Protein present at site of pathology | ||
Clusterin [14] | Clearance of cellular debris and apoptosis | -Clusterin deficiency associated with PXS. |
-Clusterin present in PXM deposits | ||
Homocysteine and human cell metabolic enzymes (MTHFR MTR, MTRR, MTHFD1, CBS) [46, 47] | Amino acids that participate in multiple metabolic processes. | Increased plasma levels associated with PXS |
It conjugates those toxic products with glutathione, protecting cells from oxidative damage | -Linkage of null genotype of the GST gene with PXS | |
Regulation of potassium channels at neuron membranes. Possible role in membrane stabilization | -CNTNAP2 gene polymorphism associated with PXS | |
Extracellular matrix maintenance | -MMP1 gene polymorphism associated with PXS | |
Adenosine receptors [45] | Adenosine regulates aqueous humor secretion. Intraocular pressure are regulated through adenosine receptors | -A3 receptor mRNA and protein selectively up regulated in eyes with PXS |
TNF-α [65] | Has dual action depending on the type of receptor activated. | -Increased expression of TNF-α shifts the balance and activates the low affinity TNF-R1 receptor leading to cell death |
 | High affinity TNF-R2 receptor has neuroprotective function while low affinity TNF-R1 receptors activation leads to cell death. |  |