I am trained as a biomedical research scientist in the field of neuroscience and ophthalmology. My doctoral research involved the pathogenesis of ischemia-induced neurodegeneration with respect to mitochondria. My doctoral studies suggested that (1) Deletion of PKC epsilon reduces neurodegeneration after global cerebral ischemia. (2) This neurodegeneration is regulated by a transcription factor (ATF2, Activation Transcription Factor 2) (3) ATF2 translocate to mitochondria and its translocation is regulated via its phosphorylation by PKC epsilon. (4) Another PKC isozyme analogous to PKC epsilon is PKC delta, which contributes to ischemia induced neurodegeneration in our study. During my postdoctoral studies under Drs. Jeffrey L. Goldberg, Yaping Joyce Liao, Ula V Jurkunas and as Instructor, I investigated the role of endoplasmic reticulum, mitochondria and oxidative stress in diseases such as ischemic optic neuropathy, diabetes retinopathy and Fuchs endothelial corneal dystrophy (FECD). My postdoctoral studies suggested that (1) Retinal ganglion cells and oligodendrocytes are selectively vulnerable to ER stress in ischemic optic neuropathy. (2) Imbalance of oxidant-antioxidant system (Loss of NQO1) causes corneal endothelial cell loss in FECD. (3) There is a loss of mitochondrial quality control in FECD which is governed by mitophagy. We are currently investigating the interaction of one stress (ER stress) with another (oxidative or mitochondria stress), which will open new avenues for the drug discovery. At Mount Sinai, I will continue my research involving ER-mitochondrial crosstalk in FECD.