Elisabeth Ferreira

High Impact

Researcher

University of Arkansas for Medical Sciences

faculty

22 h-index 51 pubs 1,637 cited

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Biography and Research Information

OverviewAI-generated summary

Elisabeth Ferreira's research program focuses on investigating molecular mechanisms underlying disease and developing novel therapeutic strategies. Her work has explored the potentiation of bone healing through gene transfer, specifically examining how IL-1Ra gene transfer can redirect osteogenesis toward endochondral ossification in conjunction with BMP2. She has also investigated the structural basis of protein interactions relevant to apoptosis, such as the sequestration of BAK by MCL-1. Another area of her research involves the study of natural compounds, like uvaol, for their potential to attenuate TGF-β1-induced epithelial-mesenchymal transition in lung cells by modulating β-catenin.

Ferreira has also contributed to the development of research tools, including a transgenic rat model designed for the noninvasive assessment of chondrogenesis <i>in vivo</i>. Her investigations extend to the synthesis and characterization of advanced materials, such as luminescent nanocomposites loaded with anti-inflammatory agents. Additionally, her publication record includes work on novel larvicides derived from cinnamamide, with evaluations of their synthesis, <i>in silico</i> properties, and <i>in vitro</i> noncytotoxicity. Her scholarly activities are reflected in an h-index of 22, with over 51 publications and 1,637 citations.

Metrics

  • h-index: 22
  • Publications: 51
  • Citations: 1,637

Selected Publications

  • Structural basis of BAK sequestration by MCL-1 in apoptosis (2025) DOI
  • CHRONIC SENESCENCE CONTRIBUTES TO FIBROCARTILAGE REPAIR IN A PRECLINICAL MODEL OF BONE MARROW STIMULATION (2024) DOI
  • IL-1Ra gene transfer potentiates BMP2-mediated bone healing by redirecting osteogenesis toward endochondral ossification (2022) DOI
  • A Transgenic Rat for Noninvasive Assessment of Chondrogenesis <i>in Vivo</i> (2021) DOI

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