Elisabeth Ferreira
Associate Scientist
Also affiliated: Centre National de la Recherche Scientifique (1996–2017); Beth Israel Deaconess Medical Center (2013–2019); Harvard University (2015–2019); Institut Pasteur (1996); Université de Lille (2010–2017); AO Foundation (2013–2016); University of Arkansas Medical Center (2025); Institut Pasteur de Lille (2013); Unité de Glycobiologie Structurale et Fonctionnelle (2007–2017); Laboratoire de Biologie, Bioingéniérie et Bioimagerie ostéoarticulaire (2004–2012); Institut de Biologie de Lille (1997–2013); Université Paris Diderot (2007); Université Lille 1 (2010); Université Lille Nord de France (2011); Eindhoven University of Technology (2012)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Elisabeth Ferreira's research focuses on cellular differentiation and the molecular mechanisms underlying tissue development and response to environmental stimuli. She has investigated the impact of hypoxia and serum deprivation on mesenchymal stem cell osteogenic differentiation and survival, as well as their angiogenic factor expression. Her work has also explored the interactions of transcription factors, such as p300, cAMP-responsive element-binding protein, and Ets-1/Ets-2, in regulating gene expression, particularly concerning the stromelysin promoter.
Further research has examined the role of osteocyte RANKL in age-related cortical bone loss and the induction of senescence. Ferreira has also contributed to the optimization of gene electrotransfer methods for mesenchymal stem cell transfection and has studied the unique mineralizing phenotype induced in mesenchymal stem cells by inflammatory cytokines. Her scholarship metrics include an h-index of 22 with 44 total publications and 1,694 total citations, designating her as a highly cited researcher.
Metrics
- h-index: 19
- Publications: 36
- Citations: 1,512
Positions
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Associate Scientist publications 2018–2025University of Arkansas for Medical Sciences Institution web page
Selected Publications
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Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation (2025)
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Structural basis of BAK sequestration by MCL-1 in apoptosis (2025)
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CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION (2024)
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IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification (2022)
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A Transgenic Rat for Noninvasive Assessment of Chondrogenesis in Vivo (2021)
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Harnessing extracellular vesicles to direct endochondral repair of large bone defects (2018)
Collaboration Network
Top Collaborators
- Harnessing extracellular vesicles to direct endochondral repair of large bone defects
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis in Vivo
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis in Vivo
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis in Vivo
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis in Vivo
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
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