Key result
Administration of Tgf-β-neutralizing antibodies abrogated non-myocyte proliferation and fibrosis in mice with hypertrophic cardiomyopathy.
Why the study?
Does inhibition of Tgf-β signaling or losartan administration prevent or reduce non-myocyte proliferation and fibrosis in HCM mouse models?
Population
HCM mouse models (mice with sarcomere protein gene mutations, including prehypertrophic and established HCM)
Comparison
Genetic ablation of periostin, administration of… vs Untreated HCM mice
Design
Preclinical
Authors
Loading...
Should not yet change HCM practice; leaves open whether Tgf-β inhibition reduces fibrosis in patients.
Does inhibition of Tgf-β signaling or losartan administration prevent or reduce non-myocyte proliferation and fibrosis in HCM mouse models?
Non-myocyte activation of Tgf-β signaling drives fibrosis in HCM, and preemptive pharmacologic inhibition with losartan or Tgf-β antibodies prevents pathologic remodeling in mouse models.
Teekakirikul et al. (2010) studied Hypertrophic cardiomyopathy. Tgf-β-neutralizing antibodies and losartan was evaluated on Non-myocyte proliferation and fibrosis. Administration of Tgf-β-neutralizing antibodies abrogated non-myocyte proliferation and fibrosis in mice with hypertrophic cardiomyopathy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: