Adipose-derived mesenchymal stem cell therapy modulates mitochondrial function to attenuate acetaminophen-induced liver injury by DDIT4/PGC-1α axis.
Cen Y., Xia C., Yao S., Weng X., Qi J., Lou G.
Prospective Study, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Stem Cell Res Ther (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41276869
- PMCID
- PMC12751710
- DOI
- 10.1186/s13287-025-04815-3
- Citations
- 1
Abstract (original English)
Background Acetaminophen (APAP) overdose is a leading cause of drug-induced liver injury, with limited treatment options. Mitochondrial dysfunction plays a central role in the pathogenesis of APAP-induced liver injury (AILI). Mitochondrial damage induces cell death, liver necrosis, and sever inflammation, leading to irreversible liver failure. Therefore, it is urgent to develop alternative treatments. Mesenchymal stem cell (MSC)-based cell therapy recently has received increasing attention for its role in regulating mitochondrial function. Objective This study aimed to investigate the regulation of mitochondrial function and the therapeutic potential of MSCs in treating AILI and underlying mechanisms. Methods AILI mouse model was established by injection of overdosed APAP. Mice were treated with adipose-derived MSCs (AMSCs) via the tail vein. The blood and liver tissues were collected for assessment of liver necrosis and mitochondrial function. To further verify the mechanism, hepatocyte-specific DNA damage-inducible transcript 4 (DDIT4) knockout (Ddit4 △Hep ) mice were generated. Results We showed that AMSCs treatment significantly reduced liver necrosis, oxidative stress, and mitochondrial dysfunction in AILI. DDIT4 expression in hepatocytes was identified as playing an important part in AMSCs treating AILI by using RNA-Seq and histological analysis. DDIT4 upregulation in liv
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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