ArticleRedox report : communications in free radical research2025
Mesenchymal stem cells enchanced by salidroside to inhibit ferroptosis and improve premature ovarian insufficiency via Keap1/Nrf2/GPX4 signaling.
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 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Isorhamnetin-preconditioned MSC-derived exosomes restore ovarian function by inhibiting ferroptosis in chemotherapy-induced POF.Stem cell research & therapy · 2026Article
- Mesenchymal stem cell therapy for premature ovarian insufficiency: progress and challenges.Journal of ovarian research · 2026Review
- Inflammatory remodeling of the ovarian microenvironment in premature ovarian insufficiency: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- SNAPIN Facilitates Progression of Hepatocellular Carcinoma by Hindering Ferroptosis Through KEAP1 Degradation Promotion.Cancer science · 2026Article
- Effects and mechanisms of MSCs and MSC-derived exosomes in regulating ferroptosis.Journal of physiology and biochemistry · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRegenerative medicine researches have shown that mesenchymal stem cells (MSCs) may be an effective treatment method for premature ovarian insufficiency (POI). However, the efficacy of MSCs is still limited. PURPOSE: This study aims to explain whether salidroside and MSCs combination is a therapeutic strategy to POI and to explore salidroside-enhanced MSCs inhibiting ferroptosis via Keap1/Nrf2/GPX4 signaling.
methodsThe effect of salidroside and MSCs on ovarian granular cells (GCs) was analyzed. After treatment, hormone levels and -fertility of rats were measured. Lipid peroxidation levels, iron deposition and mitochondrial morphology were detected. The genes and proteins of Keap1/Nrf2/GPX4 signaling were examined.
resultsSalidroside and MSCs were found to inhibit cell death of GCs by reducing peroxidation and intracellular ferrous. Salidroside promotes the proliferation of MSCs and supports cell survival in ovary. Salidroside combined with MSCs therapy restored ovarian function, which was better than MSCs monotherapy. Salidroside-enhanced MSCs to inhibit ferroptosis. The results showed activation of the Keap1/Nrf2/GPX4 signaling and an increase in anti-ferroptosis molecule.
conclusionsSalidroside-enhanced MSCs as a ferroptosis inhibitor and provide new therapeutic strategies for POI. The possible mechanisms of MSCs were related to maintaining redox homeostasis via a Keap1/Nrf2/GPX4 signaling.
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Registered trials
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