Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.

Thirty-six male mice were given angiotensin II, a chemical that causes heart stress and atrial fibrillation, and some were also treated with HNG (a version of the peptide humanin) or MOTS-c. The researchers also studied heart cells from rats in the lab, exposing them to the same chemical with or without the peptides. They measured how easily atrial fibrillation could be started in the mice, looked at heart tissue under a microscope for scarring and thickening, and checked the mitochondria, the energy-producing parts of cells, for damage. They also measured levels of inflammatory proteins and markers of cell stress. The paper reports that mice given either peptide were less likely to develop atrial fibrillation, had less scarring and thickening in the heart's upper chambers, and showed healthier mitochondria and lower inflammation compared to mice given only angiotensin II. In the rat cells, the peptides reduced stress and stopped scar-forming cells from becoming overactive. The authors note that these results are from animal and cell studies, and more work is needed before drawing conclusions about people.

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