Cited by 99Mesenchymal stem cell researchLiver physiology and pathologyLiver Disease and Transplantation

Mesenchymal stem cell therapy for liver fibrosis/cirrhosis

Open access
Cao, Yan, Ji, Chenbo, Lu, Ling·2020·Annals of Translational Medicine

Abstract

Liver fibrosis represents a common outcome of most chronic liver diseases. Advanced fibrosis leads to cirrhosis for which no effective treatment is available except liver transplantation. Because of the limitations of liver transplantation, alternative therapeutic strategies are an urgent need to find. Recently, mesenchymal stem cells (MSCs) based therapy has been suggested as an attractive therapeutic option for liver fibrosis and cirrhosis, based on the promising results from preclinical and clinical studies. Although the precise mechanisms of MSC transplantation are still not fully understood, accumulating evidence has indicated that MSCs eliminate the progression of fibrosis due to their immune-modulatory properties. In this review, we summarise the properties of MSCs and their clinical application in the treatment of liver fibrosis and cirrhosis. We also discuss the mechanisms involved in MSC-dependent regulation of immune microenvironment in the context of liver fibrosis and cirrhosis.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.21037/atm.2020.02.119

Cites

76 of 76 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • IDO metabolizes tryptophan, inducing metabolic stress that tames NK cells and promotes T cell hyperactivation while fostering regulatory immune cell populations.

    “First, through IDO, MSCs metabolize tryptophan in the local microenvironment, inducing metabolic stress that tames the ferocity of natural killer (NK) cells and promotes T cell hyperactivation while also fostering regulatory immune cell populations.”

    From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [46]

    In the sections on NK/NKT cells and T cells (page unavailable), the review reports IDO-dependent increases in regulatory NKT cells and Tregs, along with reduced NKT-cell hepatotoxicity. It does not describe tryptophan metabolism or metabolic stress as the mechanism. It also says MSCs can inhibit T-cell proliferation, contrary to the claim of T-cell hyperactivation. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • MSC-produced PGE2 converts pro-inflammatory M1 macrophages to anti-inflammatory M2, marked by decreased TNF-α and IL-6 and increased IL-10 and TGF-β.

    “Simultaneously, MSC-produced PGE2 acts as a molecular switch, converting pro-inflammatory M1 macrophages to their anti-inflammatory M2—a phenotypic shift marked by decreased harmful cytokines, such as TNF-α and IL-6, and increased healing factors, including IL-10 and TGF-β.”

    From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [46]

    The “Macrophages and KCs” section says MSC transplantation can activate M2 macrophages and inhibit M1 macrophages, and identifies TNF-α and IL-6 with M1 and IL-10 and TGF-β with M2. It does not say MSC-produced PGE2 converts M1 macrophages into M2 or demonstrate those cytokine changes during such a conversion. The “DCs” section instead describes PGE2 acting on dendritic cells. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Other sources, such as dental pulp, remain experimental due to the limited clinical data available.

    “Other sources, such as dental pulp, remain experimental due to the limited clinical data available.”

    From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [46]

    The “Sources and advantages of MSCs” section identifies dental pulp as a source of MSCs. The “Clinical trials” section names bone marrow, umbilical cord and adipose tissue as the three major sources used in liver fibrosis/cirrhosis trials. The paper does not specifically say that dental-pulp MSCs remain experimental because of limited clinical data. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • The effectiveness of these treatments is greatly influenced by matching the source to the disease stage: UC/WJ-MSCs excel in urgent advanced cases, while AD-MSCs are optimal for autologous treatment in compensated cirrhosis.

    “The effectiveness of these treatments is greatly influenced by matching the source to the disease stage: UC/WJ-MSCs excel in urgent advanced cases, while AD-MSCs are optimal for autologous treatment in compensated cirrhosis.”

    From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [46]

    The “Sources and advantages of MSCs” section says UC-MSCs may be advantageous for end-stage liver disease, but does not establish that UC/WJ-MSCs excel in urgent advanced cases. The “Clinical trials” section reports improvement after autologous AD-MSC infusion in two cirrhosis patients; its compensated-cirrhosis result instead concerns BM-MSCs. The paper calls for further study of the appropriate cell source and therapeutic window, rather than establishing the proposed stage-based choices. Page numbers were not available in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • TSG-6 suppresses neutrophil tissue entry, oxidative bursts, and pathologic neutrophil extracellular trap formation.

    “Completing this natural triad, TNF-α-stimulated gene six protein (TSG-6) is a neutrophil calmer, calming these inflammatory first responders by suppressing their tissue entry, inhibiting oxidative bursts, and preventing pathologic neutrophil extracellular trap formation [46, 47].”

    From From signaling pathways to clinical trials: mesenchymal stem cells as multimodal regenerative architects in liver cirrhosis therapy (2025) · cites this paper as [46]

    The Neutrophils section (page unavailable) discusses neutrophil infiltration and oxidative injury, but does not attribute either effect to TSG-6. Searches for TSG-6 and TNF-α-stimulated gene six found no passage addressing its effects on tissue entry, oxidative bursts, or neutrophil extracellular traps. (LLM, conf=0.75)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

1 of the 77 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [75]Thapa M, Tedesco D, Elrod E, et al. Chronic liver fibrosis triggers autoantibody production by B cells in a MyD88-dependent pathway (BA4P.126). J Immunol 2015;194:47.6.

Cited by

Sorted by citations

Authors
Cao, Y., Ji, C., & Lu, L.
Affiliations
Nanjing Maternity and Child Health Care Hospital (CN)
Corresponding author
Ji, Chenbo
Venue
Annals of Translational Medicine
Published
2020-04
Volume
8
Issue
8
Pages
562-562
ISSN
  • 2305-5839 (ISSN-L)
  • 2305-5847
OpenAlex
W3022610151
Cited by
99
References
77
Citations by year
2026: 6 · 2025: 15 · 2024: 22 · 2023: 18 · 2022: 17 · 2021: 20 · 2020: 1
FWCI
2.06
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Annals of Translational Medicine (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • Foundation of Jiangsu Collaborative Innovation Center of Biomedical Functional Materials (81971495)
  • National Natural Science Foundation of China (81971495, QNRC2016108, 81571564, BK20170152)
  • Government of Jiangsu Province
  • Natural Science Foundation of Jiangsu Province (BK20170152, BRA2017533, QNRC2016108)
  • Jiangsu Provincial Medical Youth Talent (QNRC2016108, BK20170152)
Topics
  • Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
Keywords
mesenchymal stem cells, liver fibrosis, liver cirrhosis, stem cell therapy, immunomodulation, immune microenvironment, chronic liver disease, liver transplantation alternatives

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review