AI Article Synopsis
- The adult heart primarily uses oxidative metabolism for energy, while during ischemia (like in the embryonic heart), it relies more on glycolysis.
- Deleting the sulfonylurea receptor 2 (SUR2) in adult mouse hearts protects them from injury caused by blocked and then restored blood flow.
- SUR2 deletion leads to improved glucose uptake in heart cells and indicates that targeting SUR2 could help shift cardiac metabolism to prevent heart damage.
Article Abstract
The adult myocardium relies on oxidative metabolism. In ischemic myocardium, such as the embryonic heart, glycolysis contributes more prominently as a fuel source. The sulfonylurea receptor 2 (SUR2) was previously implicated in the normal myocardial transition from glycolytic to oxidative metabolism that occurs during adaptation to postnatal life. This receptor was now selectively deleted in adult mouse myocardium resulting in protection from ischemia reperfusion injury. SUR2-deleted cardiomyocytes had enhanced glucose uptake, and SUR2 forms a complex with the major glucose transporter. These data identify the SUR2 receptor as a target to shift cardiac metabolism to protect against myocardial injury.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488756 | PMC |
| http://dx.doi.org/10.1016/j.jacbts.2018.11.012 | DOI Listing |
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