Transplanting clusters of laboratory-grown human cardiac muscle cells improved heart function in a primate model of heart attack, according to preclinical research that advances cell therapy approaches for treating heart failure.
When a heart attack occurs, affected cardiac muscle cells die due to lack of oxygen and nutrients, forming scar tissue that impairs heart function. This often leads to chronic heart failure, one of the most common causes of death in Western countries. Researchers at Hannover Medical School (MHH) are developing a therapeutic approach using biotechnologically produced heart muscle cells to repair damaged cardiac tissue.
In the study, published in Nature Communications, researchers used human induced pluripotent stem cells (hiPSCs), which can be produced from reprogrammed blood cells and differentiated into any cell type, including cardiomyocytes. Rather than injecting individual cells, the team produced spherical aggregates of cardiac muscle cells in bioreactors, hypothesising that clusters would remain in the heart and integrate more effectively than single cells.
The researchers injected these cardiac muscle cell aggregates (hiCMAs) into the hearts of Javanese macaques following induced heart attacks. Three months after treatment, extensive new human cardiac muscle fibres had formed. Although the transplants caused temporary cardiac arrhythmias, heart function improved over time.
Notably, only one of the two tested stem cell lines improved cardiac function, despite both producing similarly sized grafts. The researchers suggest that examining the contractile force of cell aggregates before transplantation may help predict therapeutic efficacy.
The team is pursuing an approach using patients’ own cells, which would eliminate the need for lifelong immunosuppressive medication. Clinical trials for safety and tolerability are still required before the therapy could become standard care.
Source: Gruh I et al. Human iPSC-cardiomyocyte-aggregate cell therapy in non-human primates and correlation of heart recovery with contractile and electrophysiological cardiomyocyte properties. Nature Communications (2026). DOI: 10.1038/s41467-026-77103-0
