Our newest publication is live!

We’re excited to announce our new Cell Reports paper, “Intramuscular adipose tissue restricts functional muscle recovery,” where we defined the functional impact of IMAT on muscle regeneration. We engineered the mFATBLOCK mouse (PdgfraCreERT2; PparγΔ/Δ in FAPs) to prevent FAP-to-adipocyte conversion—effectively blocking IMAT formation without disrupting overall metabolism or muscle homeostasis. Post-injury, mFATBLOCK mice exhibited dramatically enhanced regeneration: increased myofiber density, larger fiber cross-sectional area, and higher functional output—demonstrating IMAT is an active barrier, not just an innocent bystander. Mechanistically, we show IMAT acts as a physical impediment, limiting both nascent myofiber formation and subsequent hypertrophic growth—rather than through altered pro-myogenic signaling.

Crucially, blocking IMAT didn’t perturb FAP-derived pro-myogenic factors, immune response, or systemic leptin levels—highlighting the specificity and safety of targeting FAP adipogenesis. Special thanks to Dr. Terence Ryan and Tori in his lab for their exceptional collaboration on the functional analyses—your expertise was invaluable!  Can't wait for Tori's story to come out!