Loss of a defense protein hastened heart decline in mice
In male mice lacking the protein, heart scans at 19 months showed poorer pumping and enlarged heart chambers compared with mice with the gene intact.
Limit: The mouse experiment tested gene loss, not an age-related decline
Edited by Boris Djordjevic · AgingResearch.News
In an animal experiment, male C57BL/6 mice lacking NRF2, a protein that controls genes involved in antioxidant defenses and removing harmful substances, developed earlier heart decline than mice with the gene intact. Researchers used ultrasound scans to assess heart function at 6, 19 and 24 months. At 19 months, mice lacking NRF2 had enlarged left ventricles—the heart’s main pumping chambers—and lower measures of pumping function, indicating early heart failure. They also showed premature signs of aging and shorter lifespans.
Related analyses found lower NRF2 protein levels with age in heart muscle from male rhesus monkeys and male Fischer 344 rats. An observational analysis of heart tissue from 294 male human donors aged 20–79 found a trend toward lower NRF2 gene activity. However, this trend was not statistically significant and did not continue across all age groups.
Why it matters
Heart failure becomes more common with age. The work addresses whether changes in the heart’s antioxidant and detoxification defenses contribute to this vulnerability.
Caveats
The mouse experiment tested gene loss, not an age-related decline; NRF2 protein did not fall with age in mice with the gene intact. The experiments used male mice and do not establish the same effects in females or people.
The paper
Loss of NRF2 During Aging Contributes to Myocardial Functional Decline
University of Arizona
Antioxidants, May 27, 2026, Open access
