When starved of oxygen during a heart attack or stroke, cells unleash a flurry of emergency measures to protect themselves and the body.
When starved of oxygen during a heart attack or stroke, cells unleash a flurry of emergency measures to protect themselves and the body. For decades, scientists have observed that the body’s production of a “three-tailed” fat molecule consistently surges during this trauma but have puzzled over why. Now, Cornell researchers have uncovered its surprising role in cellular survival: protecting against damage when oxygen runs out.
The research shows that the fat molecule, N-acylphosphatidylethanolamine (NAPE), helps cells survive ischemia – oxygen loss from reduced blood flow – by driving lactic acid out of cells. This toxic byproduct builds up during emergency metabolism, and NAPE’s surge appears to be part of the body’s protective response. Though still in an early stage, the findings suggest that boosting or mimicking NAPE could one day help limit tissue damage in heart attack and stroke.
The study, published Sept. 5 in the Journal of the American Chemical Society, was led by graduate student Din-Chi Chiu and Jeremy Baskin, associate professor and Nancy and Peter Meinig Family Investigator in the Life Sciences in the Department of Chemistry and Chemical Biology in the College of Arts and Sciences, and the Weill Institute for Cell and Molecular Biology.
Read More: Cornell University
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