Lipoxygenase drives lipidomic and metabolic reprogramming in ischemic heart failure
Lipoxygenases are enzymes involved in inflammatory signaling and they do play a role in the mediation of acute and chronic heart failure (HF). What happens if a key lipoxygenase (12/15LOX) is knocked out? On the top level, survival after myocardial infarction was enhanced (89% 56 d survival in knock-out versus 58% in wild-type mice).
Changes are also reported at the molecular level: Compared to control conditions (pre-myocardial infarct), lack of 12/15LOX leads to changes in amino acid pathways with accumulation of citrulline, arginine, lysine, and spermidine in plasma. The lysine degradation product 2-aminoadipic acid is heavily decreased in concentration which already hints at a protective effect according to the authors. Acute heart failure is characterized by a heavily reorganized metabolic phenotype especially in amino acids and lipids in both 12/15LOX knock-out mice and controls. What makes this study worth reading is the detailed dissection of the metabolic pathways and the time course analysis of acute to chronic HF.
Ganesh V Halade, Vasundhara Kain, Bochra Tourki, Jeevan K Jadapalli, Lipoxygenase drives lipidomic and metabolic reprogramming in ischemic heart failure, Metabolism Clinical and Experimental, 2019 .
BACK to Cardiology