Journal of Molecular and Cellular Cardiology

Older female mice developed heart failure under combined stress

In a 15-week experiment, 19-month-old female mice developed heart failure after dietary and chemical stress, while three-month-old females did not.

Paper by Kamil Aleksander Kobak, Weronika Zarzycka, Catherine J. King, +5 more authorsYing Ann Chiao · Oklahoma Medical Research Foundation

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Mechanisms
Studied:
Experiments in 19-month-old female mice, 15 weeks, against young female mice
What changed:
Older female mice developed heart failure with preserved ejection fraction, while young female mice did not
The catch:
Did not measure whether correcting mitochondrial changes prevents heart failure
Why it’s aging research:
It studies organisms or tissues that aged naturally.

Editor of record: Boris Djordjevic · AgingResearch.News

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Researchers randomly assigned 19-month-old and three-month-old female C57BL/6JN mice to control groups or a 15-week animal experiment combining a high-fat diet with a chemical in drinking water. The diet supplied 60% of calories from fat, and the water contained 0.5 grams of the chemical per liter.

Older stressed mice developed heart failure with preserved ejection fraction: their hearts retained pumping function but had trouble relaxing. Young stressed females did not develop this condition. Older stressed mice had 40% more lung fluid than age-matched controls and ran shorter distances before exhaustion. Their heart mitochondria—the structures that supply cells with energy—functioned less well. They also showed disrupted protein maintenance, with increased mitochondrial protein production and signs of impaired disposal of damaged mitochondria.

Why it matters

Heart failure with preserved ejection fraction predominantly affects older women. Including aging in this mouse model may help researchers investigate sex-specific mechanisms of the disease.

Caveats

The findings came from experimentally induced disease in female mice, not from women with heart failure. They do not establish whether correcting the mitochondrial changes would prevent heart failure.

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