ArticleStem cell research & therapy2025
Cardioprotective effects of extracellular vesicles from hypoxia-preconditioned mesenchymal stromal cells in experimental pulmonary arterial hypertension.
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 2 papers.
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Who cites it
2 citing papers in PubMed.
- Multitarget Strategy for Treatment of Pulmonary Arterial Hypertension: Combination of Mesenchymal Cells with Novel PDE-4 Inhibitor.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Extracellular Vesicles in Alzheimer's Disease: Dual Roles in Pathogenesis, Promising Avenues for Diagnosis and Therapy.Pharmaceutics · 2026Review
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Authors and funding
17 authors.
Funding
Abstract
backgroundDuring pulmonary arterial hypertension (PAH), cardiac cells develop a hypertrophic and apoptosis-resistant phenotype. Mesenchymal stromal cell (MSC) therapy has been shown to mitigate pulmonary vascular remodeling in PAH; however, successful application is limited by low potency and the need for a high number of MSCs. MSCs exposed to hypoxia release more extracellular vesicles (EV)s with different content than normoxia. We aimed to evaluate the proteomic profile and therapeutic effects of EVs derived from normoxia- and hypoxia-preconditioned MSCs on cardiac tissue remodeling in experimental PAH.
methodsIsolated bone marrow MSCs were subjected to normoxia (N, 21%O
resultsAmong 695 proteins identified, 203 were present only in EV-H and 51 in EV-N. EV-H was enriched in proteins involved in the negative regulation of mitogen-activated protein kinase and apoptosis pathways. On day 28, both EV-N and EV-H therapies decreased RVSP compared with PAH-SAL (32 ± 5 mmHg and 29 ± 4 mmHg versus 39 ± 2 mmHg; p < 0.01). Only EV-H increased PAT/PET, reduced RV outflow diameter, and the RVH index compared with PAH-SAL. The expressions of c-Myc, a marker of myocardial injury, and p-GSK3β-Ser9, a proliferative marker, were higher in the PAH-SAL group than in the CTRL group. EV-N and EV-H decreased c-Myc expression, but only EV-H significantly reduced p-GSK3β-Ser9.
conclusionEV-N and EV-H reduced RVSP, but only EV-H improved RVH and RV outflow diameter, increased the PAT/PET ratio, and downregulated GSK3β protein levels. EVs from hypoxia-preconditioned MSCs demonstrated greater cardioprotective effects than those from normoxia-conditioned MSCs.
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