Loss of a DNA-maintenance enzyme weakens aging mouse hearts
Experiments in mice lacking the enzyme throughout their bodies found age-related heart enlargement and weaker pumping, alongside overactive signals inside heart cells.
Our read
Mechanisms- Studied:
- Experiments in mice
- In the record:
- One of 281 papers on PARP1 on record: 25 with results in people, 24 in animals.
Editor of record: Boris Djordjevic · AgingResearch.News
Mice lacking PARP1, an enzyme involved in maintaining DNA stability, developed age-related heart changes and weaker pumping in animal experiments. The researchers compared mice lacking the enzyme throughout their bodies with normal mice. Mice without PARP1 had normal heart function at two months but enlarged hearts at 14 months. PARP1 levels also declined in the hearts of aging normal mice.
Hearts lacking PARP1 showed excessive activity in Akt, a protein that relays signals inside cells. To test its role, the researchers injected 9- to 10-month-old mice with a drug that inhibits Akt at 1 milligram per kilogram of body weight daily for 14 days. The drug improved pumping in mice lacking PARP1 but did not improve heart chamber size or wall thickness.
Why it matters
Age-related heart failure involves changes in heart structure and pumping ability. The findings put PARP1’s regulation of cell signaling among the processes to investigate.
Caveats
The mice lacked PARP1 throughout their bodies, so changes outside the heart could also have contributed to their heart problems.
The paper
PARP1 deficiency induces aging-associated cardiac failure via activation of Akt signalling
Indian Institute of Science
Life Science Alliance, Nov 12, 2026
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