Fallopian tubal infertility: the result of Chlamydia trachomatis-induced fallopian tubal fibrosis.
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This review summarizes mechanisms of Chlamydia trachomatis-induced fallopian tubal fibrosis, hypothesizing that TGF signaling mediates EMT and ECM changes to cause tubal infertility.
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Abstract
Chlamydia trachomatis is one of the most common pathogens of sexually transmitted diseases, and its incidence in genital tract infections is now 4.7% in south China. Infertility is the end result of C. trachomatis-induced fallopian tubal fibrosis and is receiving intense attention from scientists worldwide. To reduce the incidence of infertility, it is important to understand the pathology-related changes of the genital tract where C. trachomatis infection is significant, especially the mechanism of fibrosis formation. During fibrosis development, the fallopian tube becomes sticky and occluded, which will eventually lead to tubal infertility. At present, the mechanism of fallopian tubal fibrosis induced by C. trachomatis infection is unclear. Our study attempted to summarize the possible mechanisms of fibrosis caused by C. trachomatis infection in the fallopian tube by reviewing published studies and further providing potential therapeutic targets to reduce the occurrence of infertility. This study also provides ideas for future research. Factors leading to fallopian tube fibrosis include inflammatory factors, miRNA, ECT, cHSP, and host factors. We hypothesized that C. trachomatis mediates the transcription and translation of EMT and ECM via upregulating TGF signaling pathway, which leads to the formation of fallopian tube fibrosis and ultimately to tubal infertility.
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