L-2-Hydroxyglutarate Protects Against Cardiac Injury via Metabolic Remodeling.
Huamei HeRyan M MulhernWilliam M OldhamWusheng XiaoYi-Dong LinRonglih LiaoJoseph LoscalzoPublished in: Circulation research (2022)
L2HGDH deletion-induced L2HG accumulation protects against myocardial injury during LFI and ischemia-reperfusion through a metabolic shift of glucose flux from glycolysis towards the pentose phosphate pathway. L2HG offers a novel mechanism for eliminating reactive oxygen species from myocardial tissue, mitigating redox stress, reducing myocardial infarct size, and preserving high-energy phosphates and cardiac function. Targeting L2HG levels through L2HGDH activity may serve as a new therapeutic strategy for cardiovascular diseases related to oxidative injury.
Keyphrases
- left ventricular
- fluorescent probe
- cardiovascular disease
- aqueous solution
- living cells
- acute myocardial infarction
- diabetic rats
- high glucose
- drug induced
- blood glucose
- type diabetes
- heart failure
- oxidative stress
- adipose tissue
- drug delivery
- skeletal muscle
- metabolic syndrome
- cardiovascular risk factors
- acute coronary syndrome