Myopia is a highly prevalent refractive error worldwide, with scleral remodeling accompanying excessive axial elongation being one of its core pathological features. As the crucial outer layer responsible for maintaining eyeball morphology and biomechanical stability, the sclera plays a decisive role in the pathogenesis and progression of myopia through abnormal alterations in its cellular components, extracellular matrix(ECM)metabolism, and regulatory networks. This review systematically summarizes recent research advances in scleral remodeling. It focuses on elucidating, from cellular and molecular perspectives, the mechanisms by which dysfunction of scleral fibroblasts, dysregulation of ECM metabolism(e.g., decreased collagen content, disrupted MMP-2/TIMP-2 balance), and complex regulatory networks involving multiple signaling pathways such as TGF-β, Wnt/β-catenin, and MAPK drive scleral thinning and reduced mechanical strength. Concurrently, the review provides a comprehensive analysis of the potential roles and existing controversies regarding factors like inflammatory responses and novel regulatory axes(e.g., FOXM1/METTL3/APOA1)in scleral remodeling. Furthermore, it discusses the current research status and application prospects of sclera-targeted intervention strategies(e.g., modulating specific pathways, supplementing exogenous factors), aiming to provide a theoretical basis and directional reference for a deeper understanding of myopia pathogenesis and the development of new prevention and treatment approaches.

Diabetic retinopathy （DR） is a common microvascular complication of diabetes mellitus， and its characteristic pathological changes include microaneurysm formation， hemorrhagic focus formation， exudate deposition， and neovascular proliferation. Long-term hyperglycemic state can induce inflammatory response， oxidative stress， and overexpression of vascular endothelial growth factor （VEGF）， which destroys the blood-retinal barrier and promotes the progression of DR. Although the current clinical treatment methods （such as laser photocoagulation and anti-VEGF drugs） have certain effects， they still have limitations， and there is an urgent need to explore safer and multi-target intervention strategies. Recent studies have discovered that the nuclear factor （NF）-κB signaling pathway plays a key role in the pathological process of DR. This pathway affects the occurrence and development of DR by regulating the release of inflammatory factors， oxidative stress response， and angiogenesis. With the advantages of multi-component， multi-target and overall regulation， traditional Chinese medicine （TCM） has shown unique potential in the prevention and treatment of DR. Especially， its precise regulation of the NF-κB pathway has become a research hotspot. This article systematically reviews the mechanisms of action of NF-κB-related signaling pathways in DR， with focuses on the research progress in TCM single herbs and active ingredients， Chinese patent medicines， and TCM compound preparations in ameliorating DR by regulating the NF-κB pathway. This review aims to provide a theoretical basis and a transformation direction for the development of drugs for the prevention and treatment of DR.

Ocular surface inflammation constitutes a core pathological mechanism underlying prevalent ocular disorders, including dry eye disease, allergic conjunctivitis, and infectious keratitis. Its pathogenesis is intimately linked to the dysregulated activation of multiple intracellular signaling cascades. This review systematically delineates the pivotal functions of four core signaling pathways—nuclear factor-kappa B(NF-κB), mitogen-activated protein kinase(MAPK), Janus kinase/signal transducer and activator of transcription(JAK/STAT), and the NOD-like receptor protein 3(NLRP3)inflammasome—in the ocular surface inflammation. Specifically, NF-κB functions as a master regulator driving the expression of pro-inflammatory factors; MAPK acts as a central signaling hub that integrates diverse stress stimuli and potentiates inflammatory amplification; JAK/STAT mediates cytokine-driven signal transduction and modulates immune cell differentiation; and NLRP3 senses danger signals and thereby promotes the maturation of inflammatory factors such as interleukin-1β(IL-1β). Notably, these pathways do not function independently but constitute a highly interconnected regulatory network via phosphorylation, and the assembly of transcription factor complexes, which results in limited efficacy of single-targeted therapies due to the reactivation of bypass pathways. Therefore, future treatment for ocular surface inflammation is expected to prioritize multi-target synergistic strategies and personalized precision medicine, thereby enabling more sustained and effective therapeutic options for clinical practice.