A signaling pathway controls heart-cell division in newborn mice
Newborn mice missing one pathway protein had hearts about 30% smaller than normal mice, with fewer heart muscle cells.
Our read
Mechanisms- Studied:
- Experiments in one-day-old mice lacking CD36, against normal mice
- What changed:
- Hearts of newborn mice lacking CD36 were about 30% smaller than normal mice, with fewer heart muscle cells
- The catch:
- Entering the cell cycle does not mean cells completed division or replaced heart muscle
- In the record:
- One of 9 papers on FABP5 on record: none yet with results in people, 3 in animals.
- Why it’s aging research:
- It studies how the body can be repaired or renewed.
Editor of record: Boris Djordjevic · AgingResearch.News
One-day-old mice lacking CD36, a cell-surface protein, had smaller hearts and fewer heart muscle cells in experiments on newborn heart growth. Their hearts failed to regenerate after researchers surgically removed the tip. The authors identified a pathway in which retinoic acid, a signaling molecule, worked through CD36 and two other proteins to control heart muscle cell multiplication.
One of those proteins, FABP5, which binds fatty acids, appeared only in heart muscle cells undergoing the cell cycle and disappeared by 9 to 11 days after birth. In adult mice, genetically reintroducing FABP5 prompted heart muscle cells to enter the cell cycle—the process cells use to divide. It also improved heart function after a heart attack.
Why it matters
Heart muscle cells lose their capacity to multiply as the heart matures. This work addresses whether restoring part of an early-life signaling program could help repair damage from interrupted blood flow.
Caveats
The adult experiments used genetically modified mice; entering the cell cycle alone does not show that cells completed division or replaced lost heart muscle. This conference abstract gives no group sizes or numerical size of the heart-function benefit.
The paper
Baylor College of Medicine
AHA Scientific Sessions 2026 Abstract, Nov 2, 2026
Presented at AHA Scientific Sessions 2026, abstract 14312
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