Elisabeth Ferreira
Researcher
Also affiliated: Centre National de la Recherche Scientifique (1985–2017); Beth Israel Deaconess Medical Center (2013–2019); Harvard University (2016–2019); Délégation Paris 7 (2007); Universidade de São Paulo (2008); Université Paris Cité (2007–2008); Université de Lille (1985–2017); AO Foundation (2013–2016); University of Arkansas Medical Center (2025); Institut Pasteur de Lille (1996); Beth Israel Deaconess Hospital (2017); Harvard University Press (2008–2015); Unité de Glycobiologie Structurale et Fonctionnelle (2007–2017); Laboratoire de Biologie, Bioingéniérie et Bioimagerie ostéoarticulaire (2008–2012); Arkansas Department of Agriculture (2025); Institut de Biologie de Lille (1997–2013); Université Lille Nord de France (2011); Eindhoven University of Technology (2012)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Elisabeth Ferreira's research focuses on understanding biological processes related to bone healing, apoptosis, and epithelial-mesenchymal transition. She has investigated the role of specific gene transfers, such as IL-1Ra, in enhancing bone regeneration by influencing osteogenesis. Her work also explores the molecular mechanisms of programmed cell death, including the interaction between BAK and MCL-1. Additionally, Ferreira studies the effects of natural compounds, like uvaol, on cellular processes, specifically its impact on TGF-β1-induced epithelial-mesenchymal transition in alveolar epithelial cells.
Her group has developed tools for noninvasive assessment of chondrogenesis, utilizing transgenic rat models. This research also extends to the synthesis and characterization of novel materials, such as luminescent nanocomposites loaded with bioactive compounds, and their anti-inflammatory effects. Furthermore, her research has explored the development of new larvicides and assessed their safety profiles.
Ferreira is recognized as a highly cited researcher, with an h-index of 22 and over 1,600 citations across 46 publications. She actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Luke Childress and Landon B. Gatrell, and has also collaborated with Bin Dong at the University of Arkansas at Fayetteville.
Metrics
- h-index: 22
- Publications: 46
- Citations: 1,681
Selected Publications
-
Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation (2025)
-
Structural basis of BAK sequestration by MCL-1 in apoptosis (2025)
-
CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION (2024)
-
IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification (2022)
-
A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i> (2021)
-
Harnessing extracellular vesicles to direct endochondral repair of large bone defects (2018)
Collaboration Network
Top Collaborators
- IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i>
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i>
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i>
- CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION
- Fibrocartilage repair involves chronic cellular senescence in a rat model of bone marrow stimulation
- A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i>
- 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
- Fibrocartilage repair involves chronic cellular senescence in a rat 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
Similar Researchers
Based on overlapping research topics