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Related Experiment Video

Updated: Dec 18, 2025

Direct Mouse Trauma/Burn Model of Heterotopic Ossification
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Activin A does not drive post-traumatic heterotopic ossification.

Charles Hwang1, Chase A Pagani1, Nanditha Das2

  • 1Department of Surgery, University of Michigan, Ann Arbor, MI, United States of America.

Bone
|June 20, 2020
PubMed
Summary
This summary is machine-generated.

Inhibiting activin A does not prevent post-traumatic heterotopic ossification (HO), unlike in fibrodysplasia ossificans progressiva (FOP). Targeting BMP pathways or ACVR1 is more effective for treating traumatic HO.

Keywords:
ACVR1ALK3-FcActivin AAnti-ACVR1 antibodyBurn tenotomyFibrodysplasia ossificans progressivaHeterotopic ossificationInhbaProgenitor cellsSingle cell RNA sequencingTrauma

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Heterotopic ossification (HO) involves ectopic bone formation in soft tissues, seen in post-traumatic HO (tHO) and fibrodysplasia ossificans progressiva (FOP).
  • Both conditions involve endochondral ossification, suggesting shared molecular pathways, particularly those involving BMP/TGFβ superfamily ligands.
  • FOP is linked to ACVR1 variants that trigger HO via activin A, a ligand not typically osteogenic for wild-type ACVR1.

Purpose of the Study:

  • To investigate the role of activin A in tHO compared to FOP.
  • To determine if activin A inhibition is a viable therapeutic strategy for tHO.

Main Methods:

  • Single-cell RNA sequencing was used to compare gene expression in tHO and FOP HO.
  • Activin A and BMP pathway gene expression was analyzed in both HO models.
  • Inhibition strategies targeting activin A, ACVR1, and osteogenic BMPs were tested in tHO models.

Main Results:

  • Activin A is expressed in response to injury in both tHO and FOP, but by distinct cell types.
  • Anti-activin A treatment did not inhibit tHO.
  • Inhibition of ACVR1 or osteogenic BMPs (using ALK3-Fc) showed some benefit in tHO but were not fully curative.

Conclusions:

  • Activin A plays a role in FOP but not in mediating tHO.
  • Inhibition of activin A is not a recommended therapeutic strategy for tHO.
  • Targeting ACVR1 or osteogenic BMPs shows potential for tHO treatment, warranting further investigation.