Rebecca G. Wells

About

Rebecca G. Wells, MD, is a Professor of Medicine (Gastroenterology) at the University of Pennsylvania School of Medicine. Her research focuses on the mechanisms of hepatic fibrosis, investigating how excess extracellular matrix is deposited by myofibroblasts derived from non-fibrogenic cells that undergo activation during chronic liver injury. She studies the role of liver stiffness and mechanical factors in fibrosis and cirrhosis, examining how mechanical properties influence myofibroblast activation and liver cell behavior. Dr. Wells's work includes exploring the contributions of matrix components such as fibronectin splice variants and proteoglycans to liver fibrosis and angiogenesis. She has demonstrated in rat models that increased liver stiffness precedes matrix deposition and that fibrosis correlates with changes in liver mechanics. Her research extends to understanding the impact of mechanical properties on hepatocellular carcinoma development, as well as studying various cell populations involved in biliary atresia and liver fibrosis. She is involved in developing comprehensive models of liver fibrosis that incorporate cellular, molecular, and mechanical factors, with the goal of advancing understanding and potential therapeutic approaches for liver diseases.

Research topics

• Cancer research
• Biology
• Political Science
• Cell biology
• Chemistry
• Biochemistry
• Internal medicine
• Genetics
• Medicine
• Immunology

Selected publications

• Promotion of cholangiocarcinoma growth by diverse cancer-associated fibroblast subpopulations

  Cancer Cell · 2021 · 399 citations

  PublisherOA PDFDOI

• Tumor restriction by type I collagen opposes tumor-promoting effects of cancer-associated fibroblasts

  Journal of Clinical Investigation · 2021-04-27 · 356 citations

  articleOpen access

  Cancer-associated fibroblasts (CAF) may exert tumor-promoting and tumor-suppressive functions, but the mechanisms underlying these opposing effects remain elusive. Here, we sought to understand these potentially opposing functions by interrogating functional relationships among CAF subtypes, their mediators, desmoplasia, and tumor growth in a wide range of tumor types metastasizing to the liver, the most common organ site for metastasis. Depletion of hepatic stellate cells (HSC), which represent…

  PublisherOA PDFDOI

• Stiff matrix induces exosome secretion to promote tumour growth

  Nature Cell Biology · 2023 · 219 citations

  DOI

• Biliary atresia

  Nature Reviews Disease Primers · 2024-07-11 · 108 citations

  reviewOpen access
  PublisherOA PDFDOI

• Cysteine-rich domain of type III collagen N-propeptide inhibits fibroblast activation by attenuating TGFβ signaling

  Matrix Biology · 2022 · 28 citations

  DOI

Recent grants

• NIH Grant R56DK092111

  NIH · $448k · 2016

• Pathological consequences of altered tissue mechanics in fibrosis

  NIH · $6.3M · 2014–2026

• NIH Grant K01MH076175

  NIH · $816k · 2012

Frequent coauthors

• Paul A. Janmey

  University of Pennsylvania

  59 shared

• Yu Du

  Fujian Agriculture and Forestry University

  43 shared

• Jessica Llewellyn

  University of Pennsylvania

  42 shared

• Matthias A. Hediger

  University Hospital of Bern

  42 shared

• Harvey F. Lodish

  Whitehead Institute for Biomedical Research

  39 shared

• Dongning Chen

  University of Pennsylvania

  37 shared

• Yoav I. Henis

  Tel Aviv University

  32 shared

• Orith Waisbourd‐Zinman

  Tel Aviv University

  29 shared

Labs

• Rebecca G. Wells LabPI

Similar researchers at University of Pennsylvania

• John Q. Trojanowskih-296
• Craig B. Thompsonh-277
• Daniel J Raderh-236