背景:大量的研究发现雌激素与肌腱病具有一定的相关性,但长期以来雌激素在肌腱病中的实验研究成果与总结较少,不方便专科从业者及相关领域学者全面了解研究近况。目的:综述目前临床或临床前原始研究,以期对雌激素在肌腱病中的作用进行总...背景:大量的研究发现雌激素与肌腱病具有一定的相关性,但长期以来雌激素在肌腱病中的实验研究成果与总结较少,不方便专科从业者及相关领域学者全面了解研究近况。目的:综述目前临床或临床前原始研究,以期对雌激素在肌腱病中的作用进行总结,并对未来雌激素在肌腱病中的评估和管理进行一定的展望。方法:通过计算机对PubMed、Web of Science、中国知网、万方和维普数据库中的相关文献进行检索。检索时间为2008年1月至2023年9月,英文检索词为“Oestrogen,Estrogen,Estrogen receptor,Tendinopathy,Tendonopathy,Sinew,Tendon,Tendons,Myotenositis”;中文检索词为“雌激素,雌激素受体,肌腱病,肌腱,肌腱炎”。依据入选标准对检索结果进行筛选排除,最终纳入60篇文献进行综述分析。结果与结论:①体内研究表明,雌激素可促进肌腱的合成代谢。也有体外实验证明多种雌激素对肌腱能够起到促进肌腱细胞增殖、减轻炎症反应和细胞凋亡的作用,但实验大都局限于动物模型。②雌激素受体β更多的在肌腱损伤和修复过程起作用,而雌激素受体α暂未发现能够在肌腱损伤过程中产生主要影响。雌激素受体β的表达通过影响脂肪形成、Ⅰ型胶原蛋白的沉积和减少肌腱细胞凋亡来修复肌腱,而其过度表达则可能会促进炎症和血管生成,从而推进炎症进程,在肌腱损伤中发挥作用。③动物研究显示,雌激素缺乏可能会降低肌腱的胶原合成效率,肌腱弹性下降,抑制肌腱的合成代谢,不利于肌腱损伤修复,而正常水平的雌激素可能对肌腱中Ⅰ型胶原合成有刺激作用,促进肌腱细胞增殖和代谢。④目前雌激素在肌腱损伤中作用的分子机制尚未完全阐释,更多实验围绕肌腱胶原合成、细胞增殖凋亡,仅有少量文献研究了雌激素受体β缺陷调控干扰素调节因子5-趋化因子配体3轴、E2调控雌激素受体α和PI-3K-A展开更多
The repair of injured tendons remains a great challenge because of the poor intrinsic healing capacity of tendons. In this study, we examined the spatiotemporal expression pattern of the bone morphogenetic protein 2 (...The repair of injured tendons remains a great challenge because of the poor intrinsic healing capacity of tendons. In this study, we examined the spatiotemporal expression pattern of the bone morphogenetic protein 2 (bmp-2) gene in normal and experimentally injured rat patellar tendons. We also investigated the ability of exogenously applied BMP-2 to promote patellar tendon healing. In situ hybridization with bmp-2 and alk-6 (bmp-2 receptor) antisense riboprobes revealed that both genes were normally expressed at low levels in intact rat tendons. However, bmp-2 expression was significantly upregulated in tenocytes found in the wound site at 7 d and later following tendon injury. In addition, it was found that bmp-2 was expressed in cultured patellar tenocytes. Appli- cation of exogenous BMP-2 to the tendon wound site significantly enhanced tendon repair. Moreover, in vitro and in vivo studies further demonstrated that BMP-2 enhanced tenocyte proliferation and migration to the wound site. The detectable amount of BMP-2 in normal tendons suggests that a basal level of bmp-2 expression was likely present to maintain the normal functions of the patellar tendon. Injury to the tendon induced increased bmp-2 expression intrinsically, but the expression level was insufficient for proper tendon repair. Our findings indicate that it is possible to significantly improve tendon healing by applying exogenous BMP-2 to the wound site, inferring that this protein could be developed as a potential therapeutic reagent for the treatment of damaged tendons.展开更多
文摘背景:大量的研究发现雌激素与肌腱病具有一定的相关性,但长期以来雌激素在肌腱病中的实验研究成果与总结较少,不方便专科从业者及相关领域学者全面了解研究近况。目的:综述目前临床或临床前原始研究,以期对雌激素在肌腱病中的作用进行总结,并对未来雌激素在肌腱病中的评估和管理进行一定的展望。方法:通过计算机对PubMed、Web of Science、中国知网、万方和维普数据库中的相关文献进行检索。检索时间为2008年1月至2023年9月,英文检索词为“Oestrogen,Estrogen,Estrogen receptor,Tendinopathy,Tendonopathy,Sinew,Tendon,Tendons,Myotenositis”;中文检索词为“雌激素,雌激素受体,肌腱病,肌腱,肌腱炎”。依据入选标准对检索结果进行筛选排除,最终纳入60篇文献进行综述分析。结果与结论:①体内研究表明,雌激素可促进肌腱的合成代谢。也有体外实验证明多种雌激素对肌腱能够起到促进肌腱细胞增殖、减轻炎症反应和细胞凋亡的作用,但实验大都局限于动物模型。②雌激素受体β更多的在肌腱损伤和修复过程起作用,而雌激素受体α暂未发现能够在肌腱损伤过程中产生主要影响。雌激素受体β的表达通过影响脂肪形成、Ⅰ型胶原蛋白的沉积和减少肌腱细胞凋亡来修复肌腱,而其过度表达则可能会促进炎症和血管生成,从而推进炎症进程,在肌腱损伤中发挥作用。③动物研究显示,雌激素缺乏可能会降低肌腱的胶原合成效率,肌腱弹性下降,抑制肌腱的合成代谢,不利于肌腱损伤修复,而正常水平的雌激素可能对肌腱中Ⅰ型胶原合成有刺激作用,促进肌腱细胞增殖和代谢。④目前雌激素在肌腱损伤中作用的分子机制尚未完全阐释,更多实验围绕肌腱胶原合成、细胞增殖凋亡,仅有少量文献研究了雌激素受体β缺陷调控干扰素调节因子5-趋化因子配体3轴、E2调控雌激素受体α和PI-3K-A
基金supported by the National Natural Science Foundation of China (30770886,30570369,30340038,30973158)National High Technology Research and Development Program of China (2007AA02Z105)+3 种基金Natural Science Foundation of Guangdong Province (04105826)Key Science and Technology Program of Guangdong Province (2004B3-0601007)Key Science and Technology Program of Guangzhou (2006Z3-E5251)the Fundamental Research Funds for the Central Universities(21609408)
文摘The repair of injured tendons remains a great challenge because of the poor intrinsic healing capacity of tendons. In this study, we examined the spatiotemporal expression pattern of the bone morphogenetic protein 2 (bmp-2) gene in normal and experimentally injured rat patellar tendons. We also investigated the ability of exogenously applied BMP-2 to promote patellar tendon healing. In situ hybridization with bmp-2 and alk-6 (bmp-2 receptor) antisense riboprobes revealed that both genes were normally expressed at low levels in intact rat tendons. However, bmp-2 expression was significantly upregulated in tenocytes found in the wound site at 7 d and later following tendon injury. In addition, it was found that bmp-2 was expressed in cultured patellar tenocytes. Appli- cation of exogenous BMP-2 to the tendon wound site significantly enhanced tendon repair. Moreover, in vitro and in vivo studies further demonstrated that BMP-2 enhanced tenocyte proliferation and migration to the wound site. The detectable amount of BMP-2 in normal tendons suggests that a basal level of bmp-2 expression was likely present to maintain the normal functions of the patellar tendon. Injury to the tendon induced increased bmp-2 expression intrinsically, but the expression level was insufficient for proper tendon repair. Our findings indicate that it is possible to significantly improve tendon healing by applying exogenous BMP-2 to the wound site, inferring that this protein could be developed as a potential therapeutic reagent for the treatment of damaged tendons.
