Advances in human umbilical cord mesenchymal stem cells-derived extracellular vesicles and biomaterial assemblies for endometrial injury treatment

Abstract

Endometrial injury caused by repeated uterine procedures, infections, inflammation, or uterine artery dysfunction can deplete endometrial stem/progenitor cells and impair regeneration, thereby diminishing endometrial receptivity and evidently lowering the live birth, clinical pregnancy, and embryo implantation rates. Currently, safe and effective clinical treatment methods or gene-targeted therapies are unavailable, especially for severe endometrial injury. Umbilical cord mesenchymal stem cells and their extracellular vesicles are characterized by their simple collection, rapid proliferation, low immunogenicity, and tumorigenicity, along with their involvement in regulating angiogenesis, immune response, cell apoptosis and proliferation, inflammatory response, and fibrosis, Therefore, these cells and vesicles hold broad potential for application in endometrial repair. This article reviewed recent research on human umbilical cord mesenchymal stem cells as well as their extracellular vesicles in repairing endometrial injury.

Keywords: Biomaterial assemblies; Endometrial injury; Extracellular vesicles; MicroRNA; Regenerative repair; Umbilical cord mesenchymal stem cells.

Figure 1

Mesenchymal stem cells and damaged endometrium. This figure illustrates the key structures of the endometrium, including the functional and basal layers, and the types of stem cells (epithelial-like and stromal-like stem cells) involved in the repair process following injury. The main sources of mesenchymal stem cells and their contribution to endometrial repair were also highlighted.

Figure 2

Mechanisms of mesenchymal stem cell-mediated repair in endometrial injury. This figure illustrates how human umbilical cord mesenchymal stem cells aid in endometrial repair through transdifferentiation, paracrine effects [via microRNAs (miRNA), exosomes, and growth factors], and immunomodulation [involving interactions with T cells, B cells, natural killer (NK) cells, and macrophages].