Scientists reverse advanced heart failure in an animal model
“We designed a mouse model to mimic the human condition of advanced heart failure,” Leach said. “Once we reproduced a severe stage of injury in the mouse heart, we inhibited the Hippo pathway. After six weeks we observed that the injured hearts had recovered their pumping function to the level of the control, healthy hearts.”
The researchers think the effect of turning Hippo off is two-fold. On one side, it induces heart muscle cells to proliferate and survive in the injured heart, and on the other side, it induces an alteration of the fibrosis. Further studies are going to be needed to elucidate the changes observed in fibrosis.
Other contributors to this paper include Todd Heallen, Min Zhang, Mahdis Rahmani, Yuka Morikawa, Matthew C. Hill, Ana Segura and James T. Willerson. The authors are affiliated with one or more of the following institutions Baylor College of Medicine, the Texas Heart Institute and Shanghai Children's Medical Center.
This study is supported by grants from the National Institutes of Health (DE023177, HL127717, HL130804, HL118761 and 5T32HL007676-23), Vivian L. Smith Foundation, State of Texas funding, Leducq Foundation Transatlantic Networks of Excellence in Cardiovascular Research (14CVD01) “Defining the genomic topology of atrial fibrillation.” Further support was provided by IDDRC grant number 1U54 HD083092 from the Eunice Kennedy Shriver National Institute of Child Health & Human Development and the Mouse Phenotyping Core at Baylor College of Medicine (U54 HG006348), the American Heart Association Scientist Development Grant (16SDG26460001) and in part by Neuroconnectivity Core and Optical Imaging and Vital Microscopy Core at Baylor College of Medicine.