David J. Goldhamer

This study identifies early transcriptional changes in fibro-adipogenic progenitors in FOP mice and shows that inhibiting ACVR1 or activin A can mitigate these changes.

The paper identifies novel enhancer elements that regulate MyoD expression during skeletal muscle development and show they are part of a cis-regulatory network.

This study shows that fascial injury, not direct muscle injury, induces heterotopic ossification in FOP by activating Acvr1R206H-expressing fibro-adipogenic progenitors, leading to muscle destruction and impaired regeneration.

The paper identifies the spatiotemporal coordination of WAVE and N-WASP with actin-bundling proteins to generate invasive protrusions during cell-cell fusion.

This study shows that an anti-ACVR1 antibody worsens heterotopic ossification in FOP mouse models by altering fibro/adipogenic progenitor behavior.

This study shows that over-expressing wild-type ACVR1 in FOP mice reduces heterotopic ossification and rescues perinatal lethality.