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Age-related macular degeneration (AMD) is currently the leading cause of vision loss in developed countries. Despite decades of research and development, there are currently no treatments for the dry version of the illness. Dry AMD (DAMD) is a multifactorial disease stemming from dysfunction in the complement system, mitochondrial function, and lipid metabolism. While the complement system has been studied in-depth for its involvement in DAMD, mitochondria and lipids are understudied for their potential contributions to this process. Ferroptosis, an iron-dependent cell death mechanism, is associated with mitochondrial dysfunction and lipid dysregulation, and has been implicated as a driver of DAMD. This review describes the pathology of DAMD and the potential role of mitochondria, metabolism, and lipid dysregulation in the disease. We will highlight the intersection of pathways involving mitochondria, lipid dysregulation, and ferroptosis in DAMD progression, as well as the need for future studies to elucidate this connection.
Dohl et al. (Thu,) studied this question.