Abstract
Evaporative dry eye disease (DED) is a common ocular condition impacting the quality of life of millions of patients worldwide. The etiology of evaporative DED is related to dysfunction of meibomian glands (MGs), resulting in suboptimal yield or lipid composition of secreted meibum. The clinical manifestation of evaporative DED involves mechanical obstruction of the MG orifice and decreased tear film stability that leads to chronic eye irritation, inflammation, and progressive damage to the cornea and surrounding tissue. Despite its high prevalence, evaporative DED remains an unmet medical need. The main obstacle in the development of effective therapeutic strategies against this disease is inadequate knowledge about the complex arrays of lipogenic reactions (meibogenesis) in the MGs and a lack of suitable animal models of the human condition. In this review, we discuss the recent advances in the creation of genetically modified mouse models that recapitulate the phenotype of evaporative DED as well as their impact on our understanding of lipid biosynthesis in MGs and therapeutic strategies targeting meibogenesis.