ArticleRedox report : communications in free radical research2025
Oxidative stress activates the transplanted adipose-derived stem cells to exert antioxidant effects in alopecia treatment.
Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosome-Based Therapies for Alopecia Areata: A Systematic Review of Clinical and Experimental Evidence.International journal of molecular sciences · 2025Pooled it
- Novel antioxidant peptides from chicken bone hydrolysate: Identification, structure-activity relationship and cytoprotective effects against oxidative stress in HaCaT cells.Food chemistry: X · 2026Article
- Advancing fat graft survival: from adipose-derived stem cell mechanisms to next-generation regenerative strategies.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlopecia is a global dermatological challenge. Adipose-derived stem cells (ADSC) show therapeutic potential, but their mechanisms in promoting hair regrowth, particularly under oxidative stress conditions, remain unclear..
objectiveTo investigate ADSC's role in promoting hair regrowth by mitigating oxidative stress.
methodsUsing H₂O₂-stressed HaCaT cells, ADSC's protective effects were evaluated via conditioned medium (CM) and co-culture. Assessments included cell viability, colony formation, ROS, MDA, antioxidant enzymes, and 8-OHdG. Nrf2 activation was analyzed by immunofluorescence and Western blot. A mouse radiation injury model validated findings.
resultsNon-pretreated ADSC offered limited oxidative protection to HaCaT cells. Conversely, H₂O₂-pretreated ADSC significantly enhanced HaCaT viability and proliferation in both CM and co-culture systems. This involved paracrine activation of the Nrf2 pathway in HaCaT cells, boosting antioxidant enzymes, accelerating ROS clearance, and reducing lipid peroxidation. These effects were reversible with Nrf2 inhibition. In vivo, CM from H₂O₂-stimulated ADSC promoted hair regrowth in irradiated mice, outperforming CM from non-pretreated ADSC by activating Nrf2 and reducing tissue oxidative damage.
conclusionsOxidative stress potentiates the protective capacity of ADSC against oxidative via Nrf2-dependent paracrine mechanisms, offering a promising strategy for alopecia treatment.
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