Abstract:Diabetic retinopathy(DR), a major microvascular complication of diabetes, is driven by hyperglycemia-induced oxidative stress, chronic inflammation, and neurodegeneration. Post-translational modifications(PTM)play pivotal roles in DR progression by dynamically regulating protein functions. Key PTMs, including phosphorylation, acetylation, ubiquitination, and O-glcNAcylation, collectively exacerbate vascular dysfunction, inflammatory responses, metabolic dysregulation, and neuronal damage. The intricate crosstalk among PTM underscores the multifaceted pathology of DR. Future research should focus on elucidating PTM interaction networks, developing targeted modulators, and leveraging advanced technologies to uncover their roles in retinal cellular heterogeneity, thereby advancing precision therapeutic strategies for DR.
