AHA Scientific Sessions 2026 Abstract

A heart support cell group sustains nerves and pumping in mice

Loss of the cell group reduced the share of blood pumped out of the left ventricle per beat from 84.0% to 68.8%.

Paper by Yiyi Yang, Katsuhito Fujiu · Institute of Science Tokyo · The Univ of Tokyo
Heart muscle sections beside a mouse contrast dense nerves and support cells in dark blue-green tissue with sparse nerves in thinner gray tissue.

Our read

Mechanisms
Studied:
Experiments in mice, against control mice
What changed:
Ejection fraction fell from 84.0 ± 1.3% to 68.8 ± 3.6% with loss of the cell group
The catch:
Only 7 mice per group in the pump function test

Editor of record: Boris Djordjevic · AgingResearch.News

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In mouse experiments, a group of fibroblasts—cells that support heart tissue—and sympathetic nerves, which help control heartbeat, depended on one another. Deleting Sema3c, a gene encoding a signaling protein, from fibroblasts reduced nerve density in the heart’s main pumping chamber. Removing a nerve cluster reduced Sema3c and Wnt gene activity in fibroblasts.

Losing the cell group also weakened pumping, in a comparison with seven mice per group. Activating Wnt signaling, a cell communication system, restored contraction in deficient mouse hearts, with nine mice per group. Blocking this signaling in healthy mouse hearts reproduced the deficit. Human heart gene-activity maps revealed a corresponding cell group. Its proportion stayed constant, but activity of the human version of Sema3c fell with aging and heart failure.

Why it matters

The authors propose that this circuit links the heart’s nerve supply to its reserve pumping capacity. Its reduced gene activity in aging and failing human hearts points to a possible role in age-related changes in heart function.

Caveats

Functional restoration was tested in mice, while human analyses measured gene activity. The conference abstract does not give the Wnt-activating drug’s dose or treatment duration.

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