This research study quantifying the changes in the metabolome, lipidome and immune profiles during acute heart failure, one day after heart attack, and during chronic heart failure, eight weeks after heart attack. So after a myocardial infarction; delayed progression or reversal of cardiac remodeling is a prime target to limit advanced chronic heart failure.
In heart failure the temporal kinetics of lipidomic and systemic metabolic signaling is unclear. But about 6 million people in the United States and 23 million worldwide; suffer from this end stage disease that involves dysfunction of the heart; a change that clinicians call cardiac remodeling.But heart failure, which comes from non resolving chronic inflammation. Over activated leukocytes from the spleen that rushed into the heart muscle to remove dead tissue; and start repairs are not adequately calming it.
But some metabolic signaling that controlling the immune responses both during the acute inflammation after injury and the resolution thereafter is important.By finding that the 12/15LOX-deficient mice bio synthesizing; the signaling molecules epoxyeicosatrienoic acids also known as EETs or cypoxins in left ventricle heart tissue after heart attack to facilitate cardiac healing.
The lipoxygenase-deficient mice also had reduced amounts of the diabetes risk bio marker 2-aminoadipic acid and had profound alterations of plasma metabolic signaling of hexoses, amino acids, biogenic amines, acylcarnitines, glycerophospholipids and sphingolipids during acute heart failure. But some specific lipoxygenase deletion alters lipidomic and metabolic signatures; with modified leukocyte profiling that delayed HF progression and improving the survival.
Specialized Pro resolving mediators
But after the myocardial infraction; lipoxygenase deriving specialized pro resolving mediators are quantifying and showing lipoxygenase deficient mice (12/15LOX−/−) bio synthesize epoxyeicosatrienoic acid (EETs; cypoxins) to facilitate cardiac healing.By this the molecular network of lipidome and metabolome in acute and chronic heart failure patients.
However, by using the genetic knock out model to delineate lipidomic, and metabolic changes to describe the role of lipoxygenase in advancing ischemic heart failure driven by leukocyte activation with signs of non resolving inflammation. Bio active lipids and metabolites are implicating in acute and chronic heart failure.