ArticleStem cell research & therapy2025
Carnosic acid serves as a dual Nrf2 activator and PTEN/AKT suppressor to inhibit traumatic heterotopic ossification.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Primary Cilia Are Required for Efficient BMP Signaling in Traumatic Heterotopic Ossification.Biomedicines · 2026Article
- Carnosic Acid Activates the STING/IRF3 Pathway to Induce Nitric Oxide-Mediated Apoptosis in Osteosarcoma Cells.Antioxidants (Basel, Switzerland) · 2026Article
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8 authors.
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Abstract
backgroundHeterotopic ossification (HO) pathogenesis involves ROS-driven stem cell differentiation. Carnosic acid (CA), a natural antioxidant, remains unexplored for HO.
methodsIn vitro, tendon-derived stem cells (TDSCs) were stimulated with IL-1β, and CA was used for intervention to assess its effects on differentiation and ROS production via real-time quantitative PCR (qPCR), western blotting (WB), and immunofluorescence. Additionally, a burn and Achilles tendon transection-induced mouse model of traumatic HO was established to evaluate the therapeutic potential of CA.
resultsIn vitro, CA activated nuclear factor erythroid 2-related factor 2 (Nrf2) and inhibited nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1), leading to increased antioxidant enzyme activity and reduced intracellular ROS levels. CA also regulated the PTEN/AKT signaling pathway, suppressing osteogenic and chondrogenic differentiation of TDSCs. In vivo, micro-computed tomography (Micro-CT) and histological analyses demonstrated that CA activated Nrf2 and enhanced antioxidant enzyme expression, thereby inhibiting osteogenic and chondrogenic factor expression in Achilles tendon tissue and reducing HO formation.
conclusionsCA is a novel HO therapeutic by dual targeting of oxidative stress and differentiation pathways.
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