ArticleMolecular & cellular proteomics : MCP2024
Circulating Autoantibody Profiling Identifies LIMS1 as a Potential Target for Pathogenic Autoimmunity in pathologic Myopia.
Article in Molecular & cellular proteomics : MCP, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Potential Ferroptosis-Related Genes and Immune Infiltration in Form-Deprivation Myopia: An Integrative Bioinformatics and in vitro Validation Study.International journal of general medicine · 2026Article
- Revisiting pathologic myopia: imaging evidence of an inflammatory component in the pathogenesis of myopic degeneration.Frontiers in medicine · 2026Review
- Plasma Metabolic Profile with Machine Learning Reveals Distinct Diagnostic and Biological Signatures for Pathologic Myopia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Preliminary insights into serum metabolomics in atrophic myopic maculopathy: potential link to fatty acid metabolism dysregulation.BMC ophthalmology · 2025Article
- The role of inflammation in myopic retinopathy.Frontiers in ophthalmology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
High myopia is a leading cause of blindness worldwide, among which pathologic myopia, characterized by typical myopic macular degeneration, is the most detrimental. However, its pathogenesis remains largely unknown. Here, using a HuProt array, we first initiated a serological autoantibody profiling of high myopia and identified 18 potential autoantibodies, of which anti-LIMS1 autoantibody was validated by a customized focused microarray. Further subgroup analysis revealed its actual relevance to pathologic myopia, rather than simple high myopia without myopic macular degeneration. Mechanistically, anti-LIMS1 autoantibody predominantly belonged to IgG1/IgG2/IgG3 subclasses. Serum IgG obtained from patients with pathologic myopia could disrupt the barrier function of retinal pigment epithelial cells via cytoskeleton disorganization and tight junction component reduction, and also trigger a pro-inflammatory mediator cascade in retinal pigment epithelial cells, which were all attenuated by depletion of anti-LIMS1 autoantibody. Together, these data uncover a previously unrecognized autoimmune etiology of myopic macular degeneration in pathologic myopia.
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