Dry Eye Disease (DED) is a multifactorial ocular surface disorder with a global prevalence ranging from 5 % to 50 % [1]. It is characterized by accelerated tear evaporation, damage to the corneal and conjunctival epithelial cells, and persistent inflammatory responses [2]. The pathogenesis of DED involves lacrimal gland dysfunction, tear film instability, and environmental factors such as excessive screen use, air pollution, and dry climates, which collectively lead to ocular surface damage and chronic inflammation [3]. Although current treatments, including artificial tears, anti-inflammatory drugs, and corneal repair therapies, provide symptomatic relief, they are insufficient for achieving systemic disease control and comprehensive tissue repair [4,5]. Uncovering the molecular mechanisms underlying DED remains a critical focus of research.

In recent years, advancements in omics technologies have provided new tools for exploring the molecular mechanisms of DED [6]. Tear proteomics, as a primary approach, has made significant progress in identifying biomarkers and pathogenic pathways, particularly those related to inflammation, immune responses, and metabolic dysregulation [[7], [8], [9]]. However, molecular alterations in tear proteomics often reflect secondary manifestations of DED, offering limited insights into the disease's root causes. The primary pathological damage in DED occurs within the corneal tissue, yet current studies have largely overlooked the proteomic characteristics of the cornea. This gap hinders a deeper understanding of the fundamental mechanisms driving DED pathogenesis.

To address this research gap, our study employs high-throughput proteomics to systematically analyze mouse corneal tissue. Unlike tear proteomics, corneal tissue directly reflects the pathological processes of DED, making it a critical target for uncovering the disease's underlying molecular mechanisms. By identifying differentially expressed proteins and validating their functions, we aim to elucidate the core pathogenic pathways of DED. Furthermore, traditional Chinese medicine (TCM), with its multi-level and multi-target regulatory mechanisms, has gained increasing attention as a potential therapeutic approach for DED [10]. The TCM formula Qingxuan Runmu Yin decoction(QXRMY)has been shown to significantly alleviate symptoms of DED by inhibiting inflammation and promoting corneal repair, thereby breaking the disease's vicious cycle at the molecular level [11]. This study integrates the intervention of QXRMY to explore its role in modulating corneal molecular pathways, providing novel theoretical foundations and therapeutic targets for the precise diagnosis and treatment of DED.The detailed process is shown in Fig. 1.