Project Details
Description
This proposal is built on the premise that newly recognized similarities between SSc and the pathways driving cellular aging, including increased CD38 expression and activity in disease that caused NAD+ depletion and SIRT activity decline, which results in unresolving myofibroblast activation and tissue fibrosis. Employing anti-CD38 antibody, by selectively blocking CD38 NADase activity, will restore NAD+ homeostasis, and prevents and reverses fibrosis in inflammation-dependent (BLM) fibrosis model. Inhibition of CD38 NADase by anti-CD38 antibody might be a novel therapy for systemic scleroderma.
| Status | Finished |
|---|---|
| Effective start/end date | 3/13/19 → 8/31/20 |
Funding
- TeneoBio, Inc. (Agmt 3/13/19)
Fingerprint
Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.