Inmaculada CerradaAmparo Ruiz‐SauríRubén CarreroCésar TriguerosAkaitz DorronsoroJosé-María Sánchez-PuellesAntonio Díez‐JuanJosé MonteroPilar Sepúlveda2026-03-222026-03-22201210.1089/scd.2012.0340https://doi.org/10.1089/scd.2012.0340https://andeanlibrary.org/handle/123456789/43457Citaciones: 87Mesenchymal stem cells (MSC) are effective in treating myocardial infarction (MI) and previous reports demonstrated that hypoxia improves MSC self-renewal and therapeutics. Considering that hypoxia-inducible factor-1 alpha (HIF-1α) is a master regulator of the adaptative response to hypoxia, we hypothesized that HIF-1α overexpression in MSC could mimic some of the mechanisms triggered by hypoxia and increase their therapeutic potential without hypoxia stimulation. Transduction of MSC with HIF-1α lentivirus vectors (MSC-HIF) resulted in increased cell adhesion and migration, and activation of target genes coding for paracrine factors. When MSC-HIF were intramyocardially injected in infarcted nude rats, significant improvement was found (after treatment of infarcted rats with MSC-HIF) in terms of cardiac function, angiogenesis, cardiomyocyte proliferation, and reduction of fibrotic tissue with no induction of cardiac hypertrophy. This finding provides evidences for a crucial role of HIF-1α on MSC biology and suggests the stabilization of HIF-1α as a novel strategy for cellular therapies.enMesenchymal stem cellBiologyAngiogenesisHypoxia (environmental)Paracrine signallingHypoxia-inducible factorsCell biologyStem cellCancer researchHIF1Aarticle