ArticleBioengineering & translational medicine2025
Reduced glutathione enhances adipose tissue-derived mesenchymal stem cell engraftment efficiency for liver fibrosis by targeting TGFβ1/SMAD3/NOX4 pathway.
Article in Bioengineering & translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The toxic footprint of lead exposure: oxido-inflammatory biomarkers in urban populations of Niger Delta, Nigeria.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Lipoaspirate-derived secretome restores redox homeostasis to attenuate pathological scar formation.Stem cell research & therapy · 2026Article
- Adipose tissue-derived mesenchymal stem cells combined with prednisone synergistically ameliorate autoimmune hepatitis in mice.Stem cell research & therapy · 2026Article
- Adipose-derived mesenchymal stromal cell-microenvironment interaction network in metabolic syndrome: ADMSC injury response, adaptive regulation, and regenerative potential.Frontiers in cell and developmental biology · 2026Review
- Mechanisms, efficacy, and future perspectives of cellular-based therapies for liver fibrosis/cirrhosis: focusing on mesenchymal stromal cells.Cell & bioscience · 2025Review
- Reduced glutathione enhances adipose tissue-derived mesenchymal stem cell engraftment efficiency for liver fibrosis by targeting TGFβ1/SMAD3/NOX4 pathway.Bioengineering & translational medicine · 2025Article
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7 authors.
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Abstract
Reduced glutathione (GSH) could reduce oxidative stress to improve adipose tissue-derived mesenchymal stem cell (ADSC) engraftment efficiency in vivo. However, the underlying mechanisms remain unclear. Our goal is to investigate whether GSH enhances ADSC engraftment through targeting the TGFβ/SMAD3/NOX4 pathway. Liver fibrotic male mice were administrated GSH, setanaxib (STX), and SIS3 during ADSC transplantation. ADSC engraftment efficiency and reactive oxygen species (ROS) level were detected both in vivo and ex vivo. Biochemical analysis was used to analyze the content of superoxide and nicotinamide adenine dinucleotide phosphate oxidases (NOXs) in liver tissues. Immunohistochemistry and western blotting were used to examine the protein level of NOX1, NOX2, NOX4, transforming growth factor-β1 (TGFβ1), SMAD3, and p-SMAD3 in liver tissues. Additionally, the therapeutic efficacy of the ADSC transplantation was further investigated. We found that GSH significantly improved ADSC engraftment efficiency, which was closely related to the reduced ROS generation in liver tissues. However, the enhanced cell engraftment was abolished after the combined treatment with STX or SIS3. GSH could effectively reduce superoxide and NOXs content, and selectively inhibit NOX4 expression in liver tissues. The co-localization results showed that GSH could reduce NOX4 expressed in activated hepatic stellate cells. Mechanistically, GSH down-regulated TGFβ/SMAD3 signaling. More importantly, GSH enhanced the therapeutic efficacy of ADSC therapy in liver fibrotic mice. Taken together, GSH could improve the engraftment efficiency of ADSCs in liver fibrosis by targeting TGFβ1/SMAD3/NOX4 signaling pathway, which provides a new theoretical basis for GSH enhancing ADSC engraftment efficiency in liver diseases.
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