Study summary · research use only
Myopia pathogenesis and vasoactive intestinal peptide: Molecular mechanisms, experimental models, and clinical implications
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review (drawing on animal models and human genetic association studies; no single species specified) discusses myopia pathogenesis and the role of vasoactive intestinal peptide (VIP) and its receptor VIPR2 in ocular growth regulation. It describes animal-model evidence in which VIP agonists or antagonists either protected from or promoted myopia depending on the model and dosage, VIPR2 knockout mice developing spontaneous myopia, and VIP interacting with circadian rhythms and atropine signaling. It also describes genetic association studies identifying VIPR2 haplotypes linked to increased or decreased myopia risk, modulated by environmental light exposure, and mechanistic work suggesting VIP is involved in choroidal and scleral remodeling alongside dopaminergic, cholinergic, and retinoic acid pathways.
Abstract
Myopia is the most common refractive error worldwide and is projected to affect half of the global population by 2050, with high myopia significantly increasing the risk of vision-threatening complications. While multiple genetic, environmental and lifestyle factors contribute to myopia onset and progression, recent findings suggest a role for vasoactive intestinal peptide (VIP) and its receptor VIPR2 in ocular growth regulation. This review summarizes current knowledge about myopia pathogenesis and the diverse factors involved, focusing on the molecular, genetic, pharmacological, and clinical findings regarding VIP/VIPR2 signaling in the eye. Evidence from animal models reveals a complex interaction between VIP and myopia, with VIP agonists/antagonists either protecting from or promoting myopia depending on model and dosage, VIPR2 knockout mice developing spontaneous myopia, and VIP interacting with circadian rhythms and atropine signaling. Genetic association studies have identified both risk and protective VIPR2 haplotypes, with environmental light exposure modulating their effects. Mechanistic studies suggest that VIP regulates choroidal and scleral remodeling, acting in concert with dopaminergic, cholinergic, and retinoic acid pathways. We propose that VIP/VIPR2 is a key modulator of emmetropization and a promising therapeutic target for myopia, though species-specific effects and context-dependency remain to be resolved.
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