Abstract
Substantive evidence demonstrates the contribution of mitochondrial dysfunction in the etiology and pathogenesis of Age-related Macular Degeneration (AMD). Recently, extensive characterization of Mitochondrial-Derived Peptides (MDPs) has revealed their cytoprotective role in several diseases, including AMD. Here we summarize the varied effects of MDPs on cellular and mitochondrial health, which establish the merit of MDPs as therapeutic targets for AMD. We argue that further research to delve into the mechanisms of action and delivery of MDPs may advance the field of AMD therapy.
Highlights
In the United States, geographic atrophy in dry AMD (Age-related Macular Degeneration) is a primary cause of vision loss in the elderly [1], and it has limited treatment options compared to those available for wet AMD [2,3]
Among the wide variety of factors that are instrumental in the etiology and pathogenesis of AMD, mitochondrial damage in the Retinal Pigment Epithelium (RPE), leading to RPE dysfunction, contributes significantly
The dry and wet forms of AMD have some common denominators in terms of AMD disease pathology, since the characteristic features of dry AMD, i.e., RPE cell apoptosis and accumulation of drusen deposits, may subsequently lead to choroidal neovascularization observed in wet AMD pathology
Summary
In the United States, geographic atrophy in dry AMD (Age-related Macular Degeneration) is a primary cause of vision loss in the elderly [1], and it has limited treatment options compared to those available for wet AMD [2,3]. The human mitochondrial genome is ~16.5 kilobases, circular, double-stranded, and consists of 37 genes that code for 13 proteins of the respiratory chain complexes These 13 proteins are a part of the electron transport chain and aid in oxidative metabolism and ATP production [8,9]. Cells 2020, 9, 1102 retrograde signaling, i.e., transmission of information from the mitochondria to the nucleus, is mediated by G-Protein Pathway Suppressor 2 (GPS2), which functions as a transcriptional activator of nuclear-encoded mitochondrial genes. The 16S rRNA gene is 1559 bp long, spanning 1671–3229 bp of the mtDNA; it occupies 1/10 of the entire mtDNA and has 413 nucleotide substitutions, which account for 25% of the 16S rRNA gene [16] Both 16S rRNA and 12S rRNA genes carry ORFs (Open Reading Frames) that encode mitochondrial-derived peptides. Numerous MDPs are well-characterized and are in preclinical development for aging-related diseases [17,18,19,20]
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