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ArticleMolecular biology reports2026

miR-26b-modified human umbilical cord mesenchymal stem cells exhibit enhanced anti-fibrotic efficacy in a mouse model of hepatic fibrosis.

Jianwei Xu, Lihong He, Jingxia Xu, Xiuzhen Yang, Wanhang Deng, Can Liu, Li Yuan, Xuxian Wu, Huanxiang Zhang

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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9 authors.

Jianwei Xu *Center for tissue Engineering and Stem Cell Research, Guizhou Medical University, Gui 'an New District, 561113, China.
Lihong He *Department of Cell Biology, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, 215123, China.
Jingxia Xu *Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Xiuzhen YangDepartment of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Wanhang DengDepartment of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
Can LiuGuizhong Biotechnology Co., Ltd, Guiyang, 550081, China.
Li YuanHaidian District Maternal and Child Health Care Hospital, Beijing, 100080, China.
Xuxian WuCenter for tissue Engineering and Stem Cell Research, Guizhou Medical University, Gui 'an New District, 561113, China. 940130341@qq.com.
Huanxiang ZhangDepartment of Cell Biology, MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, 215123, China. hzhang@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveConventional human umbilical cord mesenchymal stem cells (HUCMSCs) show insufficient liver homing and limited therapeutic efficacy against hepatic fibrosis. This work aimed to construct miR-26b-overexpressing HUCMSCs (Ad-26b-HUCMSCs) and explore their anti-fibrotic capacity and underlying mechanisms.

methodsAdenovirus was applied to achieve miR-26b overexpression in HUCMSCs. CCK-8, Transwell and flow cytometry assessed cell viability, migration and apoptosis in vitro. A CCl₄-induced mouse hepatic fibrosis model was established, with four animal groups receiving sham treatment, PBS, Ad-HUCMSCs or Ad-26b-HUCMSCs via tail vein injection. Liver function, serum cytokines, liver histopathology, cell homing and hepatic marker expression were measured 28 days post-transplantation.

resultsmiR-26b modification significantly enhanced HUCMSC viability, migratory ability and liver engraftment without increasing apoptosis. Ad-26b-HUCMSCs markedly lowered serum ALT, AST, IL-1β, IL-6 and TGF-β, relieved hepatic collagen deposition, suppressed α-SMA and TNF-α, and elevated AFP, ALB and CK18 expression in injured liver compared with unmodified HUCMSCs.

conclusionsmiR-26b overexpression improves the survival, liver-targeted migration and hepatic marker expression of HUCMSCs. Ad-26b-HUCMSCs exert potent anti-fibrotic effects, offering an optimized stem cell therapeutic strategy for hepatic fibrosis.

Indexed as

Liver CirrhosisMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMicroRNAsAnimalsApoptosisCell MovementCell SurvivalDisease Models, AnimalHumansLiverMaleMiceUmbilical CordMicroRNAsMIRN26 microRNA, humanAnti-fibrosis efficacyHuman umbilical cord mesenchymal stem cellsLiver fibrosisMigrationmiR-26b

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.