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Chuan-Ju Liu, PhD

Charles W. Ohse Professor of Orthopaedics & Rehabilitation
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Additional Titles

Vice Chair of Research, Orthopaedics & Rehabilitation

Professor, Graduate School of Arts and Sciences

About

Titles

Charles W. Ohse Professor of Orthopaedics & Rehabilitation

Vice Chair of Research, Orthopaedics & Rehabilitation; Professor, Graduate School of Arts and Sciences

Biography

Dr. Chuan-Ju Liu holds the position of Charles W. Ohse Professor of Orthopaedics, with tenure in the Traditional Track, and serves as the Vice Chair of Research for the Department of Orthopaedics & Rehabilitation at Yale University School of Medicine. Additionally, he is a Professor in the Graduate School of Arts and Sciences at Yale University. Before joining Yale, he worked at the New York University Grossman School of Medicine from 2002 to 2023, where he held various positions, including Assistant Professor, Associate Professor with tenure, and Full Professor of Orthopaedic Surgery and Cell Biology.

Dr. Liu's primary area of research is centered on critical aspects of musculoskeletal health and disorders, particularly inflammation, age-related changes in joints and bones, and skeletal diseases. His research is primarily dedicated to investigating musculoskeletal, autoimmune, and lysosomal storage diseases, with a particular emphasis on conditions like common osteoarthritis, rheumatoid arthritis, fracture healing, and rare genetic Gaucher Disease.

Dr. Liu's research contributions have resulted in the publication of approximately 200 peer-reviewed papers in esteemed journals, including Nature and Science. His research has been also recognized by multiple organizations. This includes the Kappa Delta Award from the Orthopaedic Research Society and the American Academy of Orthopaedic Surgeons, the Ethelmae Haldan Award for Innovative Science in Osteoarthritis Research from Arthritis National Research Foundation, and the Basic Research Award from American College of Rheumatology.

Appointments

Other Departments & Organizations

Education & Training

Postdoctoral Associate
Yale University School of Medicine (2000)
PhD
Shandong University & Chinese Academy of Science (1996)

Research

Overview

Arthritis is a degenerative disease that affects more than 66 million individuals in the United States alone. The destruction of the extracellular matrix of cartilage and bone is thought to be mediated by excessive proteolytic activity and an imbalance between inflammatory cytokines and their antagonists. The discovery of matrix-degrading enzymes and the inhibitors that antagonize the actions of cytokines is therefore important from both a pathophysiological and a therapeutic standpoint.

Flow Chart Demonstrating that ADAMTS-7 Plays a Role in the Progression of Osteoarthritis
We discovered that ADAMTS-7 plays a role in COMP degradation in the progression of osteoarthritis.

In the Liu Lab, our studies have led to the identification of ADAMTS-7 and ADAMTS-12 as two metalloproteinases associated with cartilage destabilization and the pathogenesis of arthritis.

In addition to our investigation into the role of ADAMTS, we have turned our attention to progranulin (PGRN), an autocrine growth factor-like molecule with multiple functions, because it was originally isolated as both a chondrogenic and osteoarthritis-related growth factor in our laboratory. Importantly, we also identified PGRN as a binding partner of tumor necrosis factor (TNF) receptors, also known as TNFRs, which are implicated in the regulation of inflammation and autoimmunity.

    Graphic Showing that Tumor Necrosis Factor Receptors are Implicated in the Regulation of Inflammation and Autoimmunity
    Tumor necrosis factor receptors are implicated in the regulation of inflammation and autoimmunity.

    Our primary focus, accordingly, is to further investigate the roles of PGRN in arthritis and autoimmune diseases, in hopes of using PGRN and its derivatives in the development of new interventions for various degenerative and inflammatory conditions.

    Series of Three Microscopic Images Showing that Progranulin is a Factor Involved in Lysosomal Storage Disorders
    We discovered that progranulin is a factor involved in lysosomal storage diseases.

    In our efforts to determine the role of PGRN in lung inflammation, we unexpectedly identified PGRN as a factor involved in Gaucher disease, one of the most common lysosomal storage diseases. Isolation of PGRN as a Gaucher disease modifier provides a foundation for future discoveries relating to this crucial factor in its disease pathogenesis, as well as in uncovering a unique target for developing novel therapies to combat Gaucher disease and probably other lysosomal storage diseases as well.

    Sodium channel Nav1.7, previously believed to be exclusive to neurons, has been identified in chondrocytes. Despite its low density, chondrocyte-expressed Nav1.7 plays a significant role in osteoarthritis progression. Genetic deletion or pharmacological inhibition of Nav1.7 reduced joint damage and alleviated joint pain in various mouse osteoarthritis models. The potential use of existing non-specific Nav blockers or Nav1.7-specific inhibitors represents an unexplored avenue for disease-modifying treatment in osteoarthritis. https://doi.org/10.1038/d41586-023-03845-2


    Medical Subject Headings (MeSH)

    Arthritis, Rheumatoid; Autoimmune Diseases; Bone Regeneration; Cartilage; Chondrocytes; Fractures, Cartilage; Inflammation; Lysosomal Storage Diseases; Musculoskeletal Development; Musculoskeletal Diseases; Musculoskeletal Pain; Osteoarthritis; Sodium Channels; Tissue Engineering

    Research at a Glance

    Yale Co-Authors

    Frequent collaborators of Chuan-Ju Liu's published research.

    Publications

    Featured Publications

    Get In Touch

    Contacts

    Academic Office Number
    Mailing Address

    Orthopaedics & Rehabilitation

    P.O. Box 208071

    New Haven, CT 06520-8071

    United States

    Administrative Support

    Locations

    • Rm0535B

      Academic Office

      Tompkins Memorial Pavilion

      789 Howard Avenue

      New Haven, CT 06519