Cystathionine-β-synthase (CBS) gene encodes L-serine hydrolyase which catalyzes 
β-reaction to condense serine with homocysteine (Hcy) by pyridoxal-5'-phosphate 
helps to form cystathionine which in turn is converted to cysteine. CBS resides 
at the intersection of transmethylation, transsulfuration, and remethylation 
pathways, thus lack of CBS fundamentally blocks Hcy degradation; an essential 
step in glutathione synthesis. Redox homeostasis, free-radical detoxification 
and one-carbon metabolism (Methionine-Hcy-Folate cycle) require CBS and its 
deficiency leads to hyperhomocysteinemia (HHcy) causing retinovascular 
thromboembolism and eye-lens dislocation along with vascular cognitive 
impairment and dementia. HHcy results in retinovascular, coronary, cerebral and 
peripheral vessels' dysfunction and how it causes metabolic dysregulation 
predisposing patients to serious eye conditions remains unknown. HHcy 
orchestrates inflammation and redox imbalance via epigenetic remodeling leading 
to neurovascular pathologies. Although circular RNAs (circRNAs) are dominant 
players regulating their parental genes' expression dynamics, their importance 
in ocular biology has not been appreciated. Progress in gene-centered analytics 
via improved microarray and bioinformatics are enabling dissection of genomic 
pathways however there is an acute under-representation of circular RNAs in 
ocular disorders. This study undertook circRNAs' analysis in the eyes of CBS 
deficient mice identifying a pool of 12532 circRNAs, 74 exhibited differential 
expression profile, ∼27% were down-regulated while most were up-regulated 
(∼73%). Findings also revealed several microRNAs that are specific to each 
circRNA suggesting their roles in HHcy induced ocular disorders. Further 
analysis of circRNAs helped identify novel parental genes that seem to influence 
certain eye disease phenotypes.