Doxorubicin-Induced Cytotoxicity in Adipose-Derived Stem Cells Is Associated With Altered SAPK/JNK Signaling.
Skubis-Sikora A., Pogoda-Mieszczak K., Sikora B., Bogunia E., Bryzek A., Czekaj P.
Animal Study, published in FASEB J (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- 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
- Animal Study
- Journal
- FASEB J (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42533549
- DOI
- 10.1096/fj.202602293R
Abstract (original English)
Adipose-derived stem cells (ADSCs) are widely used in regenerative medicine, but their functionality declines under chemotherapeutic stress. Doxorubicin (Dox) is an effective anticancer agent known to induce long-term toxicity in healthy tissues. Increasing evidence suggests that Dox promotes cellular dysfunction, including apoptosis, promotion of oxidative stress, and premature senescence. The SAPK/JNK signaling pathway is implicated in stress responses and may contribute to Dox-induced aging in stem cells. However, its role in ADSC senescence and functional decline remains unclear. This study evaluated the effects of Dox on ADSC viability and aging-associated processes, with a focus on SAPK/JNK signaling. ADSCs exposed to 0.1-100 μM Dox for 24 h showed reduced mitochondrial activity and ATP levels at clinically relevant doses (5 μM), along with disrupted cell cycle progression and cytoskeletal alterations. Dox induced both apoptosis and premature senescence and increased oxidative stress. These effects were accompanied by alterations in SAPK/JNK pathway expression. Overall, Dox promoted ADSC dysfunction, highlighting potential limitations in the therapeutic use of ADSCs during chemotherapy and emphasizing the need for protective strategies. Alterations in the SAPK/JNK signaling pathway were observed in response to Dox-induced stress, suggesting that this pathway may contribut
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.