AstraZeneca

Regenerating failing hearts

Up to one billion heart muscle cells may die as a result of reduced blood supply during a heart attack. This can lead to debilitating and often fatal heart failure.

Researchers at AstraZeneca's BioPharmaceuticals R&D organisation, in collaboration with Swedish biotech company Procella Therapeutics and medical university Karolinska Institutet, are determined to change that.

Cell therapy is a promising, rapidly advancing field with the potential to transform medicine across disease areas with significant therapeutic need. Using cell therapy to halt and reverse disease, restore damaged organs, and ultimately cure many life-threatening conditions, is now a realistic goal for scientists at the cutting edge of regenerative medicine.

In pre-clinical research, AstraZeneca has injected millions of human ventricular progenitor (HVP) cells that are capable of forming new cardiac tissue. In the laboratory, the company has seen these HVP cells develop into beating ventricular cardiomyocytes like those in a healthy heart, leading to improved cardiac function.1

 

Collaborators have also reported encouraging anti-fibrotic activity after HVP injections.2  This is important as scar tissue arising from fibrotic changes is typically seen after a heart attack and injections have been shown to reduce normal heart function.

AstraZeneca plans to fully investigate formation of ventricular cardiomyocytes following HVP cell therapy. The company wants to know how these cells integrate with muscle cells already in the heart, and how they affect tissue regeneration and cardiac function.

 

1.       Foo KS, Lehtinen ML, Leung CY et al. Human ISL1 + ventricular progenitors self-assemble into an in vivo functional heart patch and preserve cardiac function post infarction. Mol Ther. 2018; 5;26(7):1644-1659.

2.       Schneider C, Foo KS, De Angelis MT et al. Primate heart regeneration via migration and fibroblast repulsion by human heart progenitors. bioRxiv. 2020. doi: https://doi.org/10.1101/2020.07.03.183798

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