ReviewFrontiers in immunology2026
The MTRNR2L gene family and age-related macular degeneration.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
Age-related macular degeneration (AMD) is the leading cause of blindness in aging adults, yet no FDA-approved therapies exist for early and intermediate disease. Multiple interconnected pathways, including mitochondrial dysfunction, oxidative stress, and inflammation, contribute to retinal pigment epithelium (RPE) degeneration in AMD, highlighting the need for developing new cytoprotective strategies. The MTRNR2L gene family, comprising nuclear paralogs of mitochondrial-derived peptide humanin, has emerged as a potential regulator of these pathways. Humanin has demonstrated anti-apoptotic, anti-inflammatory, and mitochondrial-stabilizing effects across multiple cell types, including the RPE. Recent transcriptomic and single-cell RNA-sequencing (scRNA-seq) analyses indicate that MTRNR2L genes are upregulated in a variety of human diseases associated with cellular stress response, inflammation, angiogenesis, and neurodegeneration. These findings suggest that MTRNR2L genes participate in coordinated stress-adaptive programs and may mirror humanin's cytoprotective and immunomodulating actions. This review summarizes recent research advances and highlights key gaps for understanding the roles of the MTRNR2L family in RPE protection and AMD progression.
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