Metabolic Characterization of Ocular Tissues in Relation to Laser-Induced Choroidal Neovascularization in Rats

Age-related macular degeneration
is a metabolic compromise disorder
whose main pathological feature is choroidal neovascularization (CNV)
formation. Using untargeted metabolomics analysis, we determined to
assess the metabolomic alterations in a CNV rat model to provide an
insight into its pathogenesis. In the CNV model, there were 24 significantly
changed metabolites in the plasma and 71 in various ocular tissues.
Pathway analysis showed that certain metabolic pathways changed in
interrelated tissues: for instance, in terms of the altered urea cycle,
arginine and proline metabolism were increased in the plasma, while
spermidine and spermine biosynthesis activities were increased in
the retinal pigment epithelium (RPE)/choroid. The retina and RPE/choroid
shared the same changed metabolites of branched-chain amino acid metabolism.
Fatty acid metabolism was found to be the significant altered metabolic
pathway in the retina of this CNV model. Although the metabolism pattern
of different substances is specific for each ocular tissue, there
is also a certain material exchange between different tissues. Dysregulated
metabolomic profiles in differential tissues may point to an interconnected
pathway, oxidative stress response, which may lead to RPE cell degeneration
and, ultimately, CNV development.