For a study, researchers sought to understand that diabetic peripheral neuropathy (DPN), the most common adverse impact of diabetes, had various pathophysiological reasons, some of which were still unidentified. Diabetes can result in various problems with the cornea, including changed tear film, neuropathy, loss of sensitivity, and postponed epithelial wound healing because of the cornea’s avascularity and sensitivity to hyperglycemia. It was known as diabetic neurotrophic keratopathy (DNK), and it was a type of DPN that damages the cornea DNK. According to current research, broken epithelial-neural-immune cell interactions play a crucial role in DNK. The epithelium receives its supply via dendritic cell processes and a vast network of sensory nerve endings, and it secretes cytokines and growth factors to assist the neighboring cells. As a result, local immune cells create neurotrophic and growth factors that promote the division of neuronal and epithelial cells, respectively, while sensory nerve terminals release neuropeptides that reduce inflammation and help heal epithelial wounds. Diabetes, which also lowers dendritic cell density and inhibits sensory neuropathy and epithelial development, substantially impairs these connections. Clinically, this slows down wound healing substantially and makes it harder for sensory nerves to regenerate after injury or insult. Most DPN and DNK treatments currently available were intended to manage the disease’s severe adverse effects. The use of cell-based therapies to treat diabetic keratopathy and corneal ulcers had the potential to increase treatment efficiency.