# The Role of Granulocyte Colony-Stimulating Factor in Endometrial Preparation for Embryo Implantation in In Vitro Fertilization

**Authors:** Charalampos Voros, Fotios Chatzinikolaou, Georgios Papadimas, Iwakeim Sapantzoglou, Aristotelis-Marios Koulakmanidis, Vaitsis Dimitrios, Diamantis Athanasiou, Vasiliki Kanaka, Kyriakos Bananis, Antonia Athanasiou, Aikaterini Athanasiou, Ioannis Papapanagiotou, Charalampos Tsimpoukelis, Athanasios Karpouzos, Maria Anastasia Daskalaki, Nikolaos Kanakas, Marianna Theodora, Nikolaos Thomakos, Panagiotis Antsaklis, Dimitrios Loutradis, Georgios Daskalakis

PMC · DOI: 10.3390/life16020351 · Life · 2026-02-18

## TL;DR

This review explores how G-CSF can help prepare the endometrium for embryo implantation in IVF, showing it works best for specific patient groups.

## Contribution

The paper identifies G-CSF as a phenotype-specific endometrial conditioning strategy rather than a general IVF supplement.

## Key findings

- G-CSF reliably increases endometrial thickness in patients with thin endometrium.
- It improves implantation outcomes in patients with recurrent implantation failure through immune-stromal mechanisms.
- No benefit is observed in unselected IVF populations, highlighting the importance of patient selection.

## Abstract

Granulocyte colony-stimulating factor (G-CSF) has been suggested as a supplementary approach for endometrial preparation in IVF. Clinical results continue to be inconsistent. This narrative review synthesises molecular and clinical information to elucidate the function of G-CSF in modifying endometrial receptivity and to identify patient categories most likely to benefit. A thorough assessment was conducted on published research on G-CSF administration in women with treatment-resistant thin endometrium, recurrent implantation failure, and unselected IVF populations. The research demonstrates that G-CSF has phenotype-dependent effects. Improvements in pregnancy and live birth rates are inconsistent and seem dependent on the reversibility of underlying tissue disease; nevertheless, G-CSF reliably increases endometrial thickness in instances of thin endometrium and may restore eligibility for transfer. G-CSF improves implantation and early pregnancy outcomes in repeated implantation failure patients without modifying endometrial morphology, indicating a functional mechanism linked to immune-stromal synchronisation rather than structural expansion. In contrast, randomised controlled studies show no therapeutic benefit in unselected IVF groups. Discrepancies in research outcomes may mostly be attributed to variations in patient phenotype, initial endometrial function, and the therapy setting. Thus, G-CSF should be considered a specific approach for endometrial conditioning rather than just a supplementary component of IVF.

## Linked entities

- **Proteins:** CSF3 (colony stimulating factor 3)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, CSF3 (colony stimulating factor 3) [NCBI Gene 1440] {aka C17orf33, CSF3OS, GCSF}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, PGR (progesterone receptor) [NCBI Gene 5241] {aka NR3C3, PR}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, CEBPB (CCAAT enhancer binding protein beta) [NCBI Gene 1051] {aka C/EBP-beta, IL6DBP, NF-IL6, TCF5}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, FOXO1 (forkhead box O1) [NCBI Gene 2308] {aka FKH1, FKHR, FOXO1A}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, HOXA10 (homeobox A10) [NCBI Gene 3206] {aka HOX1, HOX1.8, HOX1H, PL}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, CSF3R (colony stimulating factor 3 receptor) [NCBI Gene 1441] {aka CD114, GCSFR, SCN7}, IL27RA (interleukin 27 receptor subunit alpha) [NCBI Gene 9466] {aka CRL1, IL-27RA, IL27R, TCCR, WSX1, zcytor1}, SOCS3 (suppressor of cytokine signaling 3) [NCBI Gene 9021] {aka ATOD4, CIS3, Cish3, SOCS-3, SSI-3, SSI3}
- **Diseases:** fibrosis (MESH:D005355), injury to (MESH:D014947), inflammation (MESH:D007249), endometriosis (MESH:D004715), vascular disease (MESH:D014652), chromosomal abnormalities (MESH:D002869), RIF (MESH:D051437), IVF (MESH:C537182), vascular insufficiency (MESH:D065666), dysregulation (MESH:D021081), genetic abnormalities (MESH:D030342), Hypoxia (MESH:D000860), Asherman syndrome (MESH:D006175), microvascular dysfunction (MESH:D017566), endometrial deficiency (MESH:D016889), immune-related dysfunction (MESH:D007154), vascular remodelling (MESH:D066253), vascular dysfunction (MESH:D002561), cytotoxicity (MESH:D064420), endometrial abnormalities (MESH:D014591), implantation (MESH:D057873), remodelling (MESH:D020257), immune dysregulation (OMIM:614878)
- **Chemicals:** oxygen (MESH:D010100), oestradiol (MESH:D004958), tyrosine (MESH:D014443), Progesterone (MESH:D011374), nitric oxide (MESH:D009569), lipid (MESH:D008055), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

96 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942483/full.md

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Source: https://tomesphere.com/paper/PMC12942483