ReviewMolecular neurodegeneration2026
Diabetic retinopathy: shaped by the "hidden hand" of post-translational modifications.
Review in Molecular neurodegeneration, 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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Abstract
Diabetic retinopathy (DR), a leading cause of vision loss in working-age adults, is increasingly recognized as a combination of neurodegenerative and microvascular disease of the retina. Its pathological mechanism is complex, involving the regulation of multiple processes such as abnormal neovascularization, nerve damage, oxidative stress, and chronic inflammation. As a key molecular mechanism for regulating protein function, post-translational modifications (PTMs) can dynamically modulate the activity and function of core cells (including retinal endothelial cells, Müller cells, and pericytes) and related signaling molecules including various forms (e.g., phosphorylation, glycosylation, acetylation, methylation, ubiquitination, and SUMOylation), thereby deeply participating in the pathological progression of DR. In addition, PTMs play a crucial role in the regulating signaling pathways, including PI3K/Akt, MAPK, AMPK, NF-κB and JAK/STAT, in the development of DR. Moreover, increasing evidence demonstrates that targeting PTMs with small molecules, either as inhibitors or activators, can reverse protein misfolding and preserve neuroretinal integrity to halt the progression of DR. This review systematically summarizes the variation characteristics of different types of PTMs in DR, analyzes the involvement of PTMs on signaling cascade and cellular processes, reviews the association between ageing and PTMs, and sorts out the research progress of PTMs as potential diagnostic biomarkers and neuroprotective therapeutic targets for DR. It aims to offer a theoretical foundation for in-depth understanding of DR pathogenesis and the development of novel prevention and treatment strategies.
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