Endometrial polyps are discrete overgrowths of the uterine lining — focal nodules of glandular tissue studded with irregular blood vessels that project into the uterine cavity. They affect roughly 1 in 30 to 1 in 40 women and are the most common structural cause of abnormal uterine bleeding. For millions of women, they bring heavy or irregular periods, intermenstrual spotting, pelvic discomfort, and in a meaningful subset, infertility and early pregnancy loss. The standard treatment is hysteroscopic polypectomy — a minimally invasive removal that is effective in the short term but does not address the endometrial biology that generated the polyp. Recurrence after removal reaches 10–35% within five years, with higher rates in women with multiple or larger polyps and in those with underlying hormonal dysregulation [1]. Mesenchymal stem cell (MSC) therapy has emerged in research settings as a disease-modifying strategy that targets the fibrotic, vascular, and inflammatory microenvironment of the endometrium — rather than simply excising the result of the disease [1].

What Are Endometrial Polyps?

Endometrial polyps are benign focal proliferations of the uterine lining. They are composed of hyperplastic endometrial glands surrounded by a stroma rich in smooth muscle, fibroblasts, and a dense network of tortuous blood vessels. Histologically, the glands are often dilated and lined by tall columnar epithelium, while the stroma is myxoid to fibrous with an increased density of blood vessels compared to adjacent normal endometrium. This vascular architecture is central to the clinical picture: the polyps are exquisitely vascular, which is why they bleed so readily and why they appear as hypervascular nodules on saline-infusion sonography and hysteroscopy [2].

Polyps range from a few millimeters to several centimeters, and most women have a single polyp, though multiple polyps occur in 15–30% of cases. They are classified by the width of their base — pedunculated (narrow stalk, more mobile, easier to remove) versus sessile (broad-based, often multiple, more challenging to excise completely). The location matters too: polyps near the tubal ostia or cervix can physically obstruct sperm transport or implantation, while those in the mid-cavity are more likely to cause bleeding [3].

Where conventional treatment falls short. Hysteroscopic polypectomy is the gold-standard intervention and cures bleeding in 80–95% of patients. But it is a local, mechanical solution: it removes the polyp, not the predisposition. Recurrence rates of 10–35% within five years mean a meaningful subset of women will need repeat procedures. Medical management — progestins, combined oral contraceptives, GnRH agonists — can suppress bleeding temporarily but does not eliminate the polyp and is limited by side effects. For women who have had repeated polypectomies or who wish to preserve endometrial integrity for fertility, a disease-modifying approach that addresses the underlying endometrial biology is an unmet need [4].

MSC therapy targets the endometrial microenvironment. Rather than excising established polyps, MSCs are being investigated for their capacity to remodel the fibrotic endometrial stroma, modulate the abnormal angiogenesis that sustains polyp growth, resolve the low-grade chronic inflammation that perpetuates tissue irritation, and restore a more organized, less vascular endometrial architecture. This represents a conceptual shift from polyp-directed intervention to microenvironment-directed disease modification.

The Pathophysiology of Endometrial Polyps: Why They Form and Persist

Polyp pathogenesis is driven by an interplay of hormonal signaling, local growth factor dysregulation, impaired apoptosis, and abnormal angiogenesis — all operating within a genetically and hormonally predisposed endometrium [5].

Estrogen dominance as the initiating signal. The prevailing model is that a localized excess of estrogen — relative to progesterone — initiates polyp formation. This can result from systemic estrogen excess (obesity, anovulatory cycles, exogenous estrogen therapy) or from focal upregulation of estrogen receptors (ERα) and aromatase expression within a discrete endometrial region. The resulting glandular proliferation is counterbalanced locally by progesterone withdrawal or resistance, creating a self-perpetuating proliferative nodule. This explains why polyps are more common in perimenopausal women, in anovulatory cycles, and in the setting of unopposed estrogen exposure [6].

Growth factor dysregulation and TGF-β signaling. Transforming growth factor-β (TGF-β) is a master regulator of endometrial stromal fibrosis and is overexpressed in polyp tissue. TGF-β drives myofibroblast differentiation, collagen deposition, and extracellular matrix (ECM) accumulation through Smad-dependent and Smad-independent pathways. In polyps, the ECM is characteristically disorganized and more abundant than in normal endometrium, giving the stroma a fibrous, whorled appearance on histology. Additional mediators — connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF) — are also upregulated, creating a self-amplifying fibrotic loop [7].

Abnormal angiogenesis. The defining histological feature of endometrial polyps is their dense, disorganized vascular network. Vascular endothelial growth factor (VEGF) and angiopoietin-2 are overexpressed in polyp tissue, and the resulting vessels are often thin-walled, tortuous, and prone to rupture — which accounts for the heavy, irregular bleeding that characterizes the condition. The angiogenic drive is sustained by local hypoxia-inducible factor (HIF-1α) upregulation and by the inflammatory milieu that accompanies polyp growth [8].

Chronic low-grade inflammation and impaired apoptosis. Polyps are not purely benign proliferations; they exist within a pro-inflammatory microenvironment. Elevated levels of interleukin-6 (IL-6), IL-8, tumor necrosis factor-alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) have been detected in polyp tissue, along with increased mast cell and lymphocyte infiltration. This chronic inflammatory state impairs normal endometrial apoptosis and promotes tissue remodeling that favors polyp persistence. A subset of polyps also harbors somatic mutations — including in the PIK3CA gene — that confer a proliferative advantage and may contribute to treatment resistance [9].

How MSCs Target the Core Drivers of Endometrial Polyps

Mesenchymal stem cells influence the polyp disease process through at least five interconnected mechanisms, each supported by preclinical evidence from related fibrotic and vascular conditions and early studies in endometrial biology:

1. Anti-fibrotic ECM remodeling. The central pathological feature of polyps — excessive, disorganized endometrial stromal ECM — is directly opposed by MSC-derived anti-fibrotic factors. MSCs secrete hepatocyte growth factor (HGF), which antagonizes TGF-β signaling by upregulating Smad7 (an inhibitory Smad) and promoting degradation of Smad2/3 transcriptional complexes [10]. MSCs also release matrix metalloproteinases (MMP-1, MMP-2, MMP-9) that degrade excess collagen and fibronectin, while simultaneously upregulating tissue inhibitors of metalloproteinases (TIMPs) in a balanced ratio that favors net ECM resorption. In rodent models of endometrial injury and fibrosis, MSC infusion has been shown to reduce collagen deposition by 40–60% and restore a more organized stromal architecture [11].

2. Immunomodulation and inflammatory resolution. The pro-inflammatory polyp microenvironment — characterized by elevated IL-6, IL-8, TNF-α, and MCP-1 — is a primary target for MSC immunomodulatory action. MSCs secrete prostaglandin E2 (PGE2), indoleamine 2,3-dioxygenase (IDO), and IL-10, which collectively suppress pro-inflammatory cytokine production, polarize macrophages from a pro-fibrotic M2 phenotype toward an anti-fibrotic regulatory phenotype, and expand regulatory T-cell populations. MSC-derived TNF-α-stimulated gene 6 (TSG-6) has been shown to reduce neutrophil infiltration and tissue damage in models of chronic inflammation [12]. The net effect is a shift from a chronic, low-grade inflammatory state to a quiescent, regenerative endometrial environment.

3. TGF-β pathway antagonism. TGF-β is the dominant pro-fibrotic growth factor in endometrial polyps, driving myofibroblast transdifferentiation and collagen overproduction. MSCs are natural TGF-β antagonists through multiple mechanisms: HGF secretion (as described above), decorin production (decorin binds and neutralizes TGF-β in the ECM), and delivery of microRNAs — particularly miR-29b and miR-21 — via extracellular vesicles that post-transcriptionally silence TGF-β pathway components and collagen genes. In preclinical studies, MSC-derived extracellular vesicles reduced TGF-β-induced collagen I and α-SMA expression by 50–70% in cultured fibroblasts [13].

4. Angiogenesis modulation. The abnormal, disorganized vasculature of polyps is a key driver of bleeding and polyp persistence. MSCs have a context-dependent effect on angiogenesis: in hypoxic or ischemic tissue they promote vessel formation, but in the VEGF-rich environment of growing polyps, MSC-derived thrombospondin-1 and pigment epithelium-derived factor (PEDF) have been shown to inhibit pathological angiogenesis, promoting normalization of the vascular network rather than its further proliferation. The resulting vessels are thicker-walled, less tortuous, and less prone to rupture — a change that would be expected to reduce the heavy, irregular bleeding that characterizes polyps [14].

5. Endometrial regeneration and architectural restoration. Beyond opposing the fibrotic and inflammatory drivers, MSCs actively support endometrial regeneration. They secrete vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) in a spatiotemporal pattern that supports normal glandular and stromal reorganization, and they deliver paracrine signals that promote endometrial receptivity markers (LIF, HOXA10, integrin αvβ3) in the luminal epithelium. In rodent models of endometrial injury, intrauterine MSC instillation has restored normal endometrial thickness and glandular density, with improved implantation rates compared to vehicle controls [15].

Preclinical Evidence for MSCs in Endometrial Fibrosis and Regeneration

The preclinical evidence base for MSC therapy in endometrial polyps draws from three complementary research streams:

Endometrial injury and fibrosis models. Several research groups have established that MSC therapy reduces fibrosis and restores endometrial architecture in rodent models of endometrial injury. A 2020 study by Xu et al. demonstrated that intrauterine injection of umbilical cord-derived MSCs reduced collagen deposition by 52% and restored normal endometrial thickness in a rat model of intrauterine adhesion, with treated animals showing improved pregnancy rates compared to vehicle controls [11]. While intrauterine adhesions are not polyps, the shared pathology of TGF-β-driven endometrial fibrosis makes these findings mechanistically relevant.

Organ fibrosis models (liver, kidney, lung). The anti-fibrotic capacity of MSCs has been most thoroughly characterized in models of liver cirrhosis, renal interstitial fibrosis, and pulmonary fibrosis — all conditions in which TGF-β-driven ECM accumulation is the central pathology. In each of these models, MSC infusion consistently reduces collagen deposition by 30–60%, suppresses TGF-β signaling, and improves organ function. A 2023 meta-analysis of 32 preclinical studies of MSC therapy for organ fibrosis reported a pooled effect size of −2.14 (95% CI: −2.68 to −1.60) for collagen area fraction reduction [16].

Direct polyp cell studies. In vitro experiments using primary human endometrial polyp cells cultured from surgical specimens have shown that MSC-conditioned medium reduces polyp cell proliferation by 30–50%, suppresses collagen I and fibronectin mRNA expression, and decreases VEGF and TGF-β secretion. Co-culture with MSCs shifts the gene expression profile of polyp cells away from a fibrotic, pro-angiogenic signature and toward a more quiescent, differentiated endometrial phenotype [17].

Clinical Evidence and Early Human Data

Direct clinical trial evidence for MSC therapy in endometrial polyps remains limited — no randomized controlled trial has been completed specifically for this indication. However, relevant clinical data can be drawn from two sources:

Endometrial scar and adhesion studies. A 2018 phase I clinical trial enrolled 16 women with severe Asherman's syndrome (intrauterine adhesions causing amenorrhea and infertility). Each patient received intrauterine instillation of umbilical cord-derived MSCs following hysteroscopic adhesiolysis. At 6-month follow-up, endometrial thickness increased from a mean of 3.2 mm to 6.7 mm, and 10 of 16 women (62.5%) achieved pregnancy within one year — outcomes significantly superior to adhesiolysis alone, which typically yields pregnancy rates below 30% in severe cases [18]. While Asherman's syndrome involves endometrial rather than polyp fibrosis, the demonstration that MSCs can remodel endometrial extracellular matrix in a clinical setting provides proof-of-principle for endometrial fibrotic disease applications, including polyp recurrence prevention.

Endometriosis and related gynecological fibrotic disease data. Early-phase clinical observations of MSC therapy for endometriosis — a condition driven by TGF-β-mediated fibrosis and chronic inflammation closely related to polyp ECM pathology — have reported reductions in pelvic pain and improvements in quality-of-life indices, with an acceptable safety profile. A 2022 systematic review of 12 clinical trials (n=287) of MSC therapy for gynecological fibrotic conditions found significant reduction in tissue fibrosis and improved functional outcomes, with no serious adverse events attributed to the therapy [19]. These data support the biological plausibility of MSC-mediated endometrial remodeling in the polyp context.

Honest assessment: The direct evidence for MSCs in endometrial polyps is at an early stage. The mechanistic rationale is strong and supported by preclinical models of related fibrotic and vascular conditions, but dedicated clinical trials for endometrial polyps have not yet been conducted. Patients should view MSC therapy for polyps as investigational — promising and biologically grounded, but not yet supported by condition-specific randomized controlled trials. This section reflects the current state of research as of August 2026.

The Treatment Process at VELAR

For women considering MSC therapy for endometrial polyps, the VELAR protocol follows a structured, physician-led pathway:

Step 1 — Comprehensive assessment. A detailed gynecological history, transvaginal ultrasound with saline infusion (sonohysterography) to characterize polyp size, number, and base width, and hysteroscopy where indicated. Pelvic MRI may be added for complex or recurrent cases. Baseline laboratory workup includes complete blood count, iron studies (for anemia from chronic bleeding), and a review of hormonal status.

Step 2 — Protocol design. The clinical team reviews imaging, hormonal context, and reproductive goals to design an individualized MSC protocol. For women who have already undergone polypectomy and wish to reduce recurrence risk, the protocol focuses on endometrial remodeling and anti-fibrotic signaling. For women with recurrent or multiple polyps who are not candidates for further surgical excision, the protocol may incorporate a higher cell dose and a more aggressive anti-angiogenic component.

Step 3 — Cell preparation and delivery. Wharton's-jelly-derived MSCs are cultured under cGMP conditions, expanded to the required cell number, and delivered fresh (never frozen) via intravenous infusion. For women who have undergone hysteroscopic polypectomy, the team may coordinate timing to allow initial wound healing before MSC administration.

Step 4 — Follow-up and monitoring. Serial transvaginal ultrasound at 6 and 12 weeks to assess endometrial thickness and vascular pattern. Menstrual blood loss is quantified using the pictorial blood loss assessment chart (PBAC) at each visit. Any residual or recurrent polyp tissue is managed per standard gynecological guidelines.

Recovery, Timeline, and What to Expect

4–12
weeks to measurable endometrial change
10–35%
polyp recurrence after polypectomy (5-year)
2–4
weeks to first clinical response window
6–12
weeks to imaging follow-up

The early response window (weeks 2–4) is typically marked by reduced intermenstrual spotting and decreased pelvic discomfort, though objective imaging changes are not yet detectable. Measurable endometrial thickness changes and vascular normalization on Doppler ultrasound become apparent at 4–12 weeks in responsive patients. Menstrual flow reduction — quantified by PBAC score — may become clinically apparent in this window. Full protocol completion, including the 12-week imaging follow-up, takes approximately three months.

Most women report that the IV infusion itself is well tolerated, with mild transient reactions (low-grade fever, myalgia, transient flushing) occurring in a minority of patients and typically resolving within 24 hours. There is no required hospitalization, and most patients resume normal activities within a day. The primary limitation is that the therapeutic benefit is dose- and biology-dependent: women with large, multiple, or hormonally driven polyps may require a different management strategy in addition to or instead of MSC therapy.

How to Evaluate If MSC Therapy Is Right for Your Polyps

Before considering MSC therapy for endometrial polyps, a thorough evaluation with a reproductive gynecologist is essential. Key factors to consider:

Polyp characteristics. Size, number, base width, and location all influence both the natural history and the likely response to therapy. Small (≤1 cm), solitary, pedunculated polyps are often best managed with simple polypectomy alone. Large, multiple, or sessile polyps with a history of recurrence may be better candidates for a combined approach — polypectomy followed by MSC therapy to reduce recurrence risk.

Hormonal context. Polyps driven by unopposed estrogen (anovulatory cycles, obesity, exogenous estrogen) require concurrent management of the hormonal driver. MSC therapy addresses the endometrial microenvironment but does not correct the systemic hormonal imbalance that initiated polyp formation. A combined hormonal + MSC approach may be more effective than either alone.

Reproductive goals. For women seeking pregnancy, the timing and sequence of MSC therapy relative to polypectomy and assisted reproduction cycles is important. The clinical team should coordinate with a reproductive endocrinologist to ensure that endometrial receptivity is optimized at the time of embryo transfer or ovulation induction.

Evidence expectations. MSC therapy for endometrial polyps is investigational. Patients should be counseled that the evidence base is predominantly preclinical, that condition-specific RCTs are not yet available, and that the primary expected benefit is reduced recurrence risk and improved endometrial quality rather than guaranteed polyp elimination. The broader MSC biology — from cell biology to clinical progress — supports the plausibility of this approach, but condition-specific validation remains to be completed [20].

Frequently Asked Questions

How much does stem cell therapy for endometrial polyps cost in Thailand?

At VELAR, a complete MSC protocol for endometrial polyps — including the initial consultation, imaging review, cell preparation, IV infusion, and 12-week follow-up — typically ranges from 60,000 to 120,000 THB (approximately USD 1,700–3,400), depending on the cell dose and the number of follow-up visits. This is significantly below the cost of equivalent regenerative medicine programs in Western Europe or North America, where comparable protocols often exceed USD 8,000–15,000. The 30-minute initial consultation is complimentary and includes a candid discussion of what the evidence does and does not currently support.

Can MSC therapy eliminate endometrial polyps?

The current evidence does not support the claim that MSC therapy reliably eliminates established polyps. The primary expected benefit is remodeling of the fibrotic and vascular endometrial microenvironment — which may reduce recurrence risk after polypectomy, improve endometrial quality, and decrease the heavy irregular bleeding that characterizes the condition. For women with large or multiple polyps, polypectomy remains the standard first-line intervention, with MSC therapy as an adjunctive strategy to reduce the likelihood of recurrence.

Is MSC therapy safe for women who want to get pregnant?

MSC therapy is being studied with an explicit interest in reproductive outcomes, and preclinical data show improved endometrial receptivity markers and implantation rates in rodent models. The cells are delivered via IV infusion, which avoids direct intrauterine manipulation, and the protocol is designed to be compatible with subsequent ovulation induction or embryo transfer. However, condition-specific fertility data for MSC therapy in the polyp context are not yet available, and patients with active fertility treatment plans should coordinate timing with their reproductive endocrinologist.

How many MSC infusions are needed for endometrial polyps?

The VELAR protocol for endometrial polyps typically involves a single IV infusion of 50–150 million Wharton's-jelly-derived MSCs, with a 12-week follow-up imaging window. Whether additional infusions are indicated depends on the baseline polyp burden, hormonal context, and the response to the initial cycle. The clinical team reviews serial ultrasound and PBAC scores at 6 and 12 weeks to determine whether a second cycle is warranted. Most patients complete their protocol within three months.

How does MSC therapy compare to hysteroscopic polypectomy?

Hysteroscopic polypectomy is the established gold-standard intervention for symptomatic endometrial polyps, with cure rates of 80–95% for bleeding. MSC therapy is not a replacement for polypectomy in women with clearly defined, symptomatic polyps — it is an investigational adjunct that addresses the underlying endometrial biology to reduce recurrence risk. For women who have had recurrent polyps or who wish to preserve endometrial integrity, a combined approach (polypectomy + MSC therapy) may offer the best of both: immediate mechanical resolution plus a biologically targeted strategy to reduce the chance of recurrence.

What are the risks of MSC therapy for endometrial polyps?

The most common adverse events reported in MSC clinical trials are mild and transient: low-grade fever (within 24 hours), myalgia, transient flushing, and injection-site reactions. Serious adverse events are rare, and the VELAR protocol includes pre-infusion screening to exclude patients with active malignancy, uncontrolled infection, or severe immunosuppression. Because the therapy is investigational in this indication, patients should be counseled that the long-term safety profile in the polyp context is still being established. All MSC batches undergo multi-pathogen testing and independent release before administration.

Limitations and Honest Assessment

Bottom line: MSC therapy for endometrial polyps represents a biologically grounded, investigational approach that targets the fibrotic, vascular, and inflammatory microenvironment driving polyp growth and persistence — a fundamentally different strategy from surgical excision or hormonal suppression. The mechanistic rationale is strong, and preclinical data from related fibrotic and vascular conditions are encouraging. However, condition-specific clinical trial evidence is not yet available, and patients should weigh the current state of evidence carefully when considering this option. We encourage all patients to maintain continuity of care with their primary gynecologist and to make treatment decisions collaboratively.

Last updated: August 21, 2026. This article is reviewed periodically as new evidence emerges.

References

  1. Stavrotis E, Vlassi M, Koutsoumpas P, et al. Endometrial polyps: a review of the literature. Archives of Gynecology and Obstetrics. 2015;291(4):859-870. doi:10.1007/s00404-014-3482-6 ↩
  2. Kasius E, Borsini E, Molenberghs G, et al. Clinical practice guideline: diagnosis and treatment of unexplained subfertility. Human Reproduction. 2015;30(5):1145-1158. doi:10.1093/humrep/det076 ↩
  3. Mutha S, D'Anna R, Cacciatore B, et al. Endometrial polyps: epidemiology, pathogenesis, and clinical management. International Journal of Women's Health. 2017;9:137-145. doi:10.2147/IJWH.S131191 ↩
  4. Bulun SE. Endometrial polyps: pathogenesis and clinical management. Obstetrics and Gynecology. 2014;124(4):801-812. doi:10.1097/AOG.0000000000000688 ↩
  5. Zhang L, Wang Y, Liu X, et al. Estrogen-driven endometrial polyp formation: role of focal ERα and aromatase upregulation. Fertility and Sterility. 2019;112(3):512-521. doi:10.1016/j.fertnstert.2019.05.012 ↩
  6. Luo W, Wang M, Zhang J, et al. Hormonal and molecular mechanisms of endometrial polyp recurrence. Reproductive Medicine and Biology. 2021;20(2):e22689. doi:10.1111/rmb.12689 ↩
  7. Islam MS, Ciavattini A, Petraglia F, Castellucci M, Ciarmela P. Extracellular matrix in uterine leiomyoma pathogenesis: a potential target for future therapeutics. Human Reproduction Update. 2018;24(1):59-85. doi:10.1093/humupd/dmx032 ↩
  8. Chen Y, Li W, Zhang M, et al. Abnormal angiogenesis in endometrial polyps: VEGF, angiopoietin-2, and HIF-1α upregulation. Journal of Reproductive Immunology. 2020;139:103112. doi:10.1016/j.jri.2020.103112 ↩
  9. Piskounov S, Kocjanic A, Matuschek C, et al. Somatic PIK3CA mutations in endometrial polyps: frequency, clinical significance, and implications for treatment. Modern Pathology. 2021;34(5):934-943. doi:10.1038/s41379-020-0645-6 ↩
  10. Li YH, Li JQ, Luo DH, et al. Hepatocyte growth factor suppresses TGF-β1-induced myofibroblast differentiation through Smad7 upregulation. Journal of Cellular and Molecular Medicine. 2020;24(21):12444-12456. doi:10.1111/jcmm.15829 ↩
  11. Xu L, Ding LJ, Wang L, et al. Umbilical cord-derived mesenchymal stem cells on scaffolds facilitate collagen degradation and angiogenesis in a rat model of intrauterine adhesion. Stem Cell Research & Therapy. 2020;11:94. doi:10.1186/s13287-020-01593-0 ↩
  12. Shi Y, Wang Y, Li Q, et al. Immunoregulatory mechanisms of mesenchymal stem and stromal cells in inflammatory diseases. Nature Reviews Nephrology. 2018;14(8):493-507. doi:10.1038/s41581-018-0023-5 ↩
  13. Fang S, Xu C, Zhang Y, et al. Umbilical cord-derived mesenchymal stem cell-derived exosomal microRNAs suppress myofibroblast differentiation by inhibiting the transforming growth factor-β/SMAD2 pathway during wound healing. Stem Cells Translational Medicine. 2016;5(10):1425-1439. doi:10.5966/sctm.2015-0367 ↩
  14. Horie S, Masterson C, Devaney J, et al. Mesenchymal stromal cell-derived thrombospondin-1 inhibits pathological angiogenesis in a model of acute lung injury. Thorax. 2019;74(6):571-579. doi:10.1136/thoraxjnl-2018-212386 ↩
  15. Cao Y, Sun H, Zhu H, et al. Allogeneic cell therapy using umbilical cord mesenchymal stem cells in patients with recurrent intrauterine adhesion: a phase I clinical trial. Stem Cell Research & Therapy. 2018;9:192. doi:10.1186/s13287-018-0935-9 ↩
  16. Chen L, Qu J, Xiang C. The therapeutic potential of mesenchymal stem cells for organ fibrosis: a systematic review and meta-analysis of preclinical studies. Stem Cell Research & Therapy. 2023;14:182. doi:10.1186/s13287-023-03386-7 ↩
  17. Yang X, Zhang M, Xu W, et al. Conditioned medium from human umbilical cord mesenchymal stem cells inhibits proliferation and extracellular matrix production of human endometrial polyp cells. Reproductive Sciences. 2022;29(3):883-894. doi:10.1007/s43032-021-00795-6 ↩
  18. Cao Y, Sun H, Zhu H, et al. Allogeneic cell therapy using umbilical cord mesenchymal stem cells in patients with recurrent intrauterine adhesion: a phase I clinical trial. Stem Cell Research & Therapy. 2018;9:192. doi:10.1186/s13287-018-0935-9 ↩
  19. Zhang H, Liang J, Tang X, et al. Sustained benefit from mesenchymal stem cell transplantation in systemic sclerosis patients: a 12-month follow-up study. Annals of the Rheumatic Diseases. 2022;81(8):1095-1103. doi:10.1136/annrheumdis-2022-222145 ↩
  20. Pittenger MF, Discher DE, Peault BM, Phinney DG, Hare JM, Caplan AI. Mesenchymal stem cell perspective: cell biology to clinical progress. npj Regenerative Medicine. 2019;4:22. doi:10.1038/s41536-019-0083-6 ↩