2024, Vol. 28 ›› Issue (32): 5231-5237

Research progress in the effect of estrogen on tendinopathy

Sun Qingfeng1, Bai Shuo2, Zhang Zhen3, Shen Liang4, Gao Beiyao5, Ge Ruidong5   

Abstract: BACKGROUND: Increasing studies have found that estrogen has a certain correlation with tendinopathy, but for a long time, there are few experiments and summaries of estrogen in tendinopathy, which makes it difficult for specialists and scholars in related fields to fully understand the research status.
OBJECTIVE: To summarize the current clinical or preclinical original research, so as to summarize the role of estrogen in tendinosis, and make a certain prospect for the evaluation and management of estrogen in tendinosis in the future.
METHODS: Relevant literature in PubMed, Web of Science, CNKI, WanFang, and VIP databases were searched by computer. Search time was from January 2008 to September 2023. The search terms were “oestrogen, estrogen, estrogen receptor, tendinopathy, tendonopathy, sinew, tendon, tendons, myotenositis” in English and “estrogen, estrogen receptor, tendinosis, tendon, tendinitis” in Chinese. According to the selection criteria, the search results were screened and excluded, and finally 60 documents were included for review and analysis.
RESULTS AND CONCLUSION: In vivo studies have shown that estrogen can promote tendon anabolism. In vitro experiments have also proved that various estrogens can promote the proliferation of tendon cells and reduce inflammation and apoptosis, but most of the experiments are limited to animal models. Estrogen receptor β acts more in tendon injury and repair processes, but estrogen receptor α has not been found to have a major impact on tendon injury. The expression of estrogen receptor β can repair the tendon by affecting the formation of fat, the deposition of type I collagen and reducing the apoptosis of tendon cells, while its over-expression may promote inflammation and angiogenesis, thus promoting the inflammatory process and playing a role in tendon injury. Animal studies have shown that estrogen deficiency may reduce the synthesis efficiency of collagen in the tendon, decrease the elasticity of tendon, inhibit the synthesis and metabolism of the tendon, which is not conducive to the repair of tendon injury, while normal level of estrogen may stimulate the synthesis of type I collagen in tendon and promote the proliferation and metabolism of tendon cells. At present, the molecular mechanism of estrogen in tendon injury has not been fully explained. More experiments focus on tendon collagen synthesis, cell proliferation and apoptosis. Only a few documents have studied the molecular mechanisms of estrogen receptor β deficiency regulating interferon regulatory factor 5-chemokine ligand 3 axis, E2 regulating estrogen receptor α and PI-3K-Akt signaling pathways, and high levels of estradiol reducing the level of free-circulating insulin-like growth factor. Various estrogens, including endogenous estrogens and phytoestrogens, are beneficial to the repair of tendinopathy at normal levels, and estrogen receptor β mainly affects the formation of fat, the deposition of type I collagen and the reduction of apoptosis of tendon cells through, which lays a foundation for the future treatment of tendinopathy with different subtypes of estrogens in vivo and the influence of estrogen membrane receptors on tendinopathy.

Key words: estrogen subtype, estrogen receptor, estrogen level, tendinopathy, tendon injury, tendinitis, biomechanical characteristics, proliferation and differentiation, molecular mechanism, review