New publication in PLOS ONE

Ischemic heart disease is the major cause of death worldwide. When adult humans suffer a heart attack the damaged muscle does not regenerate. Instead, a build-up of permanent scar tissue prevents heart repair, reducing cardiac performance, leading to death in the long term. Over recent years, researchers have explored heart injury in various animal models to understand the process of scarring and repair so as to provide therapies for damaged hearts.

Our team looked at heart injury in adult frogs (Xenopus laevis), a previously uncharacterised model. Now frogs can be used to compare injury responses with models that can and cannot regenerate the heart, and provide leads as to the mechanisms involved.  We found that the responses were similar to adult mammals (i.e. humans). Almost one year after injury, heart cardiomyocyte cells remained hypertrophic (increased in size) and were not properly organised like uninjured hearts, additionally the organ tissue remained scarred. We hope that future work with this model will help to understand mechanisms in heart scarring and ways to help regeneration following cardiac injury.

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Endoscopic ventricle biopsy procedure in adult frogs induces a fibrous scar with absence of heart regeneration.

Endoscopic procedure in anesthetised frog allows “in situ” live visualisation of the operating field and collection ventricle tissue in the apical region using biopsy forceps. The resulting outcome for the frog heart is the induction of scar related gene expression during the first week post-amputation (SHORT TERM) and the establishment of a persistent fibrous scar, cardiac hypertrophy and sarcomere disorganisation at the amputation site, without the capacity for the cardiac tissue to regenerate, even after almost one year (LONG TERM).

© 2017 Marshall et al.

Marshall L., Vivien C., Girardot F., Péricard L., Demeneix B.A., Coen L., Chai N. (2017) Persistent fibrosis, hypertrophy and sarcomere disorganisation after endoscopy-guided heart resection in adult Xenopus. PLoS One, 9;12(3):e0173418. doi: 10.1371/journal.pone.0173418.