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The R21 and R56 grants will fund the study of a genetic variant associated with high risk of OA, and how cartilage changes during aging, respectively.

The long-term goal of the Diekman lab is to elucidate the biology of aging as a way to catalyze new therapeutic strategies for OA.

The awarded grants support this goal in two different ways:

  • The R21 grant provides two years of funding for “high risk / high reward” projects. Dr. Diekman’s team will study a small genetic change that encodes an extra-cellular matrix protein known as chondroadherin-like (Chadl). While rare, those with this genetic risk factor are nearly 8-times as likely to have a total hip replacement due to OA. Understanding how this change accelerates the aging of cartilage will lead to a better understanding of this process across patients of all genetic backgrounds.
  • The R56 grant provides one year of funding to enable a project to begin while applying for long-term R01 funding. Dr. Diekman has teamed up with Dr. Richard Loeser and Dr. Jeremy Purvis to study the how chondrocytes change during aging. Chondrocytes that become senescent are thought to contribute to the loss of cartilage, but more work is needed in order to selectively eliminate these cells as a treatment for OA.

The preliminary phases of these projects were supported by numerous institutional sources – NC TraCS, the Comparative Medicine Institute, TARC, the UNC School of Medicine Office of Research, the UNC Office of the Executive Vice Chancellor and Provost, and the Department of Biomedical Engineering that is joint across UNC and NCSU.

For those who are interested in joining the team, there is a temporary research technician position open in Dr. Diekman’s lab: Click here to apply

Links and additional information:

Diekman Lab
Loeser Lab
Purvis Lab
Comparative Medicine Institute
UNC/NCSU Department of Biomedical Engineering

R21 Grant: “Functional follow-up of a genetic variant associated with high risk of osteoarthritis,” NIAMS, #1R21AR077821-01A1

R56 Grant: “Understanding the role of cellular senescence in osteoarthritis: dynamics, clearance, and mechanisms of induction,” NIA, #1R56AG066911-01A1