Research progress on the mechanism of estrogen deficiency on lacrimal gland fibrosis

Fibrosis is a process characterized by excessive accumulation of extracellular matrix. This process is initiated by long-term chronic inflammatory response and a variety of pathogenic factors. It is closely related to inflammatory response and tissue regeneration, and plays a role in defense and repair of tissues or organs. However, it becomes an uncontrolled and irreversible pathological fibrosis in the case of continuous damage to tissues or organs. Estrogen is a natural antioxidant, and estrogen therapy is considered to be a reliable treatment for anti-oxidation, which can fight against inflammatory and traumatic clinical symptoms of many diseases. Estrogen deficiency can cause the accumulation of inflammatory cells in lacrimal gland tissue, accelerate the degenerative changes of lacrimal gland tissue, promote the occurrence of inflammation and fibrosis of lacrimal gland tissue, and affect the morphology, immune response and function of lacrimal gland tissue. However, the specific mechanism of the occurrence and development of lacrimal gland tissue fibrosis is still unclear. In clinical practice, lacrimal gland fibrosis is not sensitive to the first-line treatment drug glucocorticoid response, resulting in repeated episodes of lacrimal gland inflammatory infiltration and delayed healing, which seriously affects the quality of life of patients. This article reviews the mechanism and research status of estrogen deficiency in lacrimal gland fibrosis from the aspects of tear production, the effect of estrogen deficiency on lacrimal gland fibrosis-related diseases, the relationship between epithelial-mesenchymal transition of lacrimal gland cells and lacrimal gland fibrosis, and the possible mechanism of estrogen deficiency leading to cell senescence and lacrimal gland fibrosis, so as to provide reference for related research and clinical application.