Objective To establish an ideal transfer strategy by investigating the relationships among embryo transfer (ET) depth, endometrial thickness, and subsequent in vitro fertilization treatment clinical pregnancy outcomes. Methods In the present retrospective analysis, data from in vitro fertilization‐ET treatment cycles conducted at a fertility center in Shanghai, China, between October 2014 and March 2015 were analyzed. Women were divided into groups 1–4 according to transfer depth (<10; 10–15, 15–20, and >20 mm, respectively), as measured by air bubbles. Additionally, 391 women were divided into groups A–C according to endometrial thickness (<7, 1–12, and >12 mm, respectively). Clinical pregnancy outcomes were assessed by group. Results Data from 501 cycles were included. Clinical pregnancy and live delivery rates were significantly higher in group 2 (P=0.009 and P=0.002, respectively) and group 3 (P=0.008 and P=0.001, respectively) than in group 4. Among the 394 patients with endometrial thickness data available, clinical pregnancy and live delivery rates were higher in group B (P=0.028 and P=0.015, respectively) and group (P=0.013 and P=0.013, respectively) than in group A. Conclusion Correct transfer depth and endometrial thickness can increase the rates of clinical pregnancy, implantation, and live delivery. Placing the embryos at 10–20 mm from the fundus and at an endometrial thickness of more than 7 mm is recommended for optimal clinical pregnancy outcomes.

Objective: To evaluate whether endometrial thickness (EMT) change in response to progesterone has an effect on pregnancy outcomes in frozen-thawed embryo transfer (FET) cycles.

Background: Thin endometrial tissue is a leading cause of embryo transfer failure, potentially contributing to sustained infertility and associated adverse outcomes. The application of exosomes derived from autologous or allogeneic bone marrow-derived stem cells (BMSCs) has been used to promote uterine repair following injury, and there is also prior evidence that stem cell transplantation can bolster fertility. Genetic modifications represent a primary approach to enhancing exosomal therapy strategies. The present study thus explored the effects of Cardiotrophin-1 (CTF1)-modified BMSCs-exo on fertility-related outcomes.Methods: An adenoviral vector was used to generate CTF1-overexpressing BMSCs (C-BMSCs), after which exosomes were isolated from control BMSCs (BMSC-exos) and C-BMSCs (C-BMSC-exos). The angiogenic effects of C-BMSC-exo treatment were assessed through analyses of endothelial cell proliferation and tube formation. Model rats exhibiting endometrial thinning were administered C-BMSCs-exo, after which the effects of such treatment were assessed through H&amp;E staining, Masson’s trichrome staining, and immunofluorescence analyses. The mechanistic basis for the proangiogenic effects of CTF1 as a driver of endometrial regeneration was additionally explored.Results: C-BMSC-exo treatment of HUVECs was associated with enhanced neovascularization, as evidenced by improved in vitro proliferation, migration, and tube formation. Importantly, such treatment was also linked to tissue regeneration, neovascularization, and the suppression of localized tissue fibrosis in vivo. Regenerated endometrial tissue exhibited higher embryo receptivity and was associated with higher birth rates in treated rats. The upregulation of the JAK/PI3K/mTOR/STAT3 signaling pathways in C-BMSC-exo-treated rats may underscore the mechanistic basis whereby CTF1 can positively impact endometrial angiogenesis and regeneration.Conclusion: Our data suggest that exosomes produced by CTF1-modified BMSCs can more effectively promote the regeneration of endometrial and myometrial tissues, driving neovascularization in a manner that improves endometrial receptivity in a rat model system, highlighting the therapeutic promise of this approach for patients diagnosed with endometrial thinning.