Pterygium is a relatively common ocular surface disease that is characterized by the growth of fibrovascular tissue from the conjunctiva to the central cornea. A relatively small pterygium can cause corneal astigmatism that can affect vision, and if the pterygium tissue continues to grow and obscure the visual axis, it can cause significant visual impairment. Pterygium can pose a serious threat to vision, and there is a lack of prevention and cure for pterygium, so research on its pathogenesis has been a hot topic in ocular surface disease research. In recent years, the discovery of abnormal expression of several tumor-related genes in pterygium and the tumor-like biological behavior of pterygium have led researchers to believe that pterygium is an abnormal proliferative disease of the ocular surface, which has led to a greater interest in the study of the pathogenesis of pterygium. 1. A review of the literature on pterygium published in Pubmed in recent years. The pathogenesis of pterygium is still unknown to date. A variety of factors have been found to contribute to this ocular disease that grows only on the human ocular surface and for which no satisfactory animal models have been established. (1) Oxidative damage and abnormal proliferation: The eye is one of the most UV-sensitive parts of the body, and the cornea and conjunctiva on the ocular surface are more susceptible to UV damage than the intraocular tissues. According to epidemiological surveys, a variety of ocular surface lesions, such as pterygium, climacteric small-drop keratopathy, and corneal intraepithelial neoplasia formation, are associated with UV exposure. Pterygium occurs most often in people who work outdoors, and a high incidence has been extensively documented in fishermen, farmers, and offshore oil workers. The harmful effects of UV radiation come from direct phototoxicity and the formation of oxygen radicals. Damage to DNA can lead to mutations and loss of heterozygotes, resulting in cell proliferation and genomic instability.28, 29 8-hydroxydeoxyguanosine (8-OHdG) is a sensitive and stable biological indicator for evaluating oxidative DNA damage. A significant increase of 8-OHdG in pterygium tissue compared to normal conjunctiva can be found by immunohistochemistry and correlates with the abnormal increase of p53 protein detected in pterygium specimens. p53 tumor suppressor gene is the most common mutated gene found in human tumors. In normal cells, p53 protein is a transiently present protein that is maintained at low, barely detectable levels. mutations in the p53 gene will result in a significant increase in the amount of p53 protein in the cell and thus be detectable. mutations in the p53 gene, modifications or mutations in the regulatory region, methylation of important regions, or defects in regulators of gene expression may result in silencing of the p53 gene. The failure to detect irreparable DNA damage or replication errors in a timely manner leads to the accumulation of this damage or errors and causes mutations in potentially oncogenic genes.30 Following the finding of abnormally high p53 expression in pterygium, p63 (a homolog of p53) and p16 (an oncogene) have also been shown to be abnormally expressed in pterygium tissue.31-33 On the other hand, oxygen free radicals can cause mutations in p53 by activating NF -kB (Nuclearfactor kB) signaling pathway to generate cyclooxygenase 2 (COX 2). Unlike cyclooxygenase 1 (COX1), which is expressed in almost all normal tissues, COX-2 can be produced in the presence of various tumor promoters. In studies of UV-associated skin cancer models, studies on the role of COX-2 include: enhanced production of prostaglandin E 2, which acts as a promoter to initiate cell proliferation; inhibition of apoptosis, leading to retention of UV-damaged cells; alteration of cell-matrix attachment thereby predisposing them to tumorigenesis; and increased DNA adducts or reduced DNA repair. cox2 is also a key player in causing inflammatory cytokine COX2 is also a key enzyme in inflammatory cytokine production and neovascularization.34, 35 (2) Abnormal neovascularization: The process of neovascularization refers to the formation of new blood vessels from an already existing vascular system. Physiological neovascularization is widespread during physiological changes such as growth and development, ovulation, and wound healing. Pathological neovascularization, on the other hand, is widespread in tumor growth and in many serious ocular diseases. A study of microvessel density (MVD) in surgically excised specimens revealed that pterygium tissue had a significantly higher MVD than normal bulbar conjunctival tissue. This is an aspect of pterygium that is more inclined to tumor tissue. Many mechanisms such as activation of cell-derived neovascularization factors, synthesis of extracellular matrix and migration of endothelial cells are involved in the neovascularization process. For example, VEGF (vascular endothelial growth factor), TNF-a (tumour necrosis factor-a), bFGF (basic fibroblast growth factor), PDGF (platelet-derived growth (basic fibroblast growth factor), PDGF (platelet-derived growth factor), and TGF-b (transforming growth factor-b). Immunohistochemistry showed that these growth factors are located in epithelial cells, vascular endothelial cells, basement membrane, fibroblasts and infiltrating inflammatory cells of pterygium. Among them, the action of VEGF is considered to be the most potent and specific. This heparin-binding glycoprotein has an important role in vascular endothelial cells, promoting endothelial cell division, increased vascular permeability, and cell proliferation and migration. Hypoxia and stimulation of certain cytokines can lead to VEGF production. High levels of VEGF expression in pterygium tissue are well documented.36 Eph receptors are receptor tyrosine kinases (RTKs), and the Eph receptor and its ligand ephrin are required for early remodeling of the embryonic vascular system. Numerous studies have found that it is also involved in the neovascularization of tumors.37, 38 The role of Eph receptors and their ligand ephrin has also been found in diabetic retinopathy, retinopathy of prematurity, and corneal neovascularization.39, 40 The molecular biology of Eph/ephrin on neovascularization is just beginning to be studied, and there are many questions to explore. Preliminary studies have found that it is also involved in the neovascularization mechanism of pterygium. （The matrix metalloproteinases (MMPs) are type IV collagenases with a relative molecular mass of 9.2×104, which can degrade type IV collagen and laminin, components of the basement membrane with a unique helical structure, and disrupt the integrity of the substrate. . Several studies have shown that the expression of MMP-9 promotes the formation of tumor neovascularization and promotes tumor invasion and metastasis. Several studies have shown that the MMP family plays an important role in the development of pterygium, and that UVB irradiation and stimulation by certain growth factors leads to the production of MMP-1, which is resistant to interstitial fibrillar collagen, a major component of the corneal extracellular matrix. Studies have demonstrated that MMP-1 shows high expression in pterygium tissue, which may be related to the ability of pterygium tissue to invade the cornea.41 (4), Viral infection: Some scholars believe that humanpapillomavirus (HPV) infection is also a relevant factor in the development of pterygium, the results of which are not yet clear.Rodrigues et al. examined a group of pterygium specimens In an earlier study, also using PCR, HPV DNA was not amplified in pterygium specimens.43 In a study of herpes simplex virus (HSV) and pterygium specimens, HPV DNA was not amplified in pterygium specimens. In a study of the correlation between herpes simplex virus (HSV) and pterygium, no significant correlation was found.44 In summary, the pathogenesis and development of pterygium is still not fully understood, and multiple pathophysiologic and molecular biological mechanisms are involved, which remain to be further investigated and explored. Identifying these mechanisms may allow us to develop pharmacological treatments for pterygium to prevent its occurrence or progression, rather than just allowing it to develop and then using surgical excision.