Mesenchymal stromal cells: promising treatment for liver cirrhosis
Open accessAbstract
Liver fibrosis is a wound-healing process that occurs in response to severe injuries and is hallmarked by the excessive accumulation of extracellular matrix or scar tissues within the liver. Liver fibrosis can be either acute or chronic and is induced by a variety of hepatotoxic causes, including lipid deposition, drugs, viruses, and autoimmune reactions. In advanced fibrosis, liver cirrhosis develops, a condition for which there is no successful therapy other than liver transplantation. Although liver transplantation is still a viable option, numerous limitations limit its application, including a lack of donor organs, immune rejection, and postoperative complications. As a result, there is an immediate need for a different kind of therapeutic approach. Recent research has shown that the administration of mesenchymal stromal cells (MSCs) is an attractive treatment modality for repairing liver injury and enhancing liver regeneration. This is accomplished through the cell migration into liver sites, immunoregulation, hepatogenic differentiation, as well as paracrine mechanisms. MSCs can also release a huge variety of molecules into the extracellular environment. These molecules, which include extracellular vesicles, lipids, free nucleic acids, and soluble proteins, exert crucial roles in repairing damaged tissue. In this review, we summarize the characteristics of MSCs, representative clinical study data, and the potential mechanisms of MSCs-based strategies for attenuating liver cirrhosis. Additionally, we examine the processes that are involved in the MSCs-dependent modulation of the immune milieu in liver cirrhosis. As a result, our findings lend credence to the concept of developing a cell therapy treatment for liver cirrhosis that is premised on MSCs. MSCs can be used as a candidate therapeutic agent to lengthen the survival duration of patients with liver cirrhosis or possibly reverse the condition in the near future.
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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 [47]
The Characteristics of MSCs section states that MSC-secreted PGE2 transforms pro-inflammatory M1 macrophages into anti-inflammatory M2 macrophages. The Immunomodulatory effects section separately reports decreased TNF-α and IL-6 and increased IL-10 after MSC treatment, but does not identify those changes as markers of the PGE2-driven shift. It also does not report increased TGF-β as part of that shift. Page numbers were unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIDO 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 [47]
The Characteristics of MSCs and Immunomodulatory effects sections (pages not provided) link MSC-produced IDO to immune suppression and describe MSCs inhibiting NK cells and fostering regulatory T cells. They do not describe tryptophan metabolism or metabolic stress as the mechanism. The claim that IDO promotes T-cell hyperactivation is especially unsupported: the paper associates IDO with reduced T-cell proliferation or activation, while describing enhanced T-cell responses under different conditions. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTSG-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 [47]
The Immunomodulatory effects section discusses MSC-mediated inflammation and neutrophil infiltration, but does not address TSG-6’s effects on neutrophils. Searches for TSG-6, oxidative bursts, and neutrophil extracellular traps found no passage supporting the attributed mechanisms; the paper provides no page numbers for these passages. (LLM, conf=0.76)
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Stem cells for hepatic regeneration: Evaluating mechanisms, sources, and clinical outcomes
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- Authors
- Yao, L., Hu, X., Dai, K., Yuan, M., Liu, P., Zhang, Q., & Jiang, Y.
- Affiliations
- Renmin Hospital of Wuhan University (CN)
- Corresponding author
- Jiang, Yingan
- Venue
- Stem Cell Research & Therapy
- Published
- 2022-07-15
- Volume
- 13
- Issue
- 1
- Pages
- 308-308
- ISSN
- 1757-6512 (ISSN-L)
- PMC
- PMC9284869
- OpenAlex
- W4285591414
- Cited by
- 71
- References
- 116
- Citations by year
- 2026: 21 · 2025: 25 · 2024: 15 · 2023: 9 · 2022: 1
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Stem Cell Research & Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- The National Natural Science Foundation of China (81972673)
- 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 cirrhosis, liver fibrosis, cell therapy, liver regeneration, extracellular vesicles, immunomodulation, hepatocyte differentiation, paracrine signaling, extracellular matrix deposition, hepatotoxicity
- MeSH terms
- Humans, Liver Cirrhosis, Liver Regeneration, Mesenchymal Stem Cell Transplantation, Mesenchymal Stem Cells
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