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With its extensive network of receptors throughout the human body that has intricate functions in the nervous system, immune system, and all of the body's other organs, the endocannabinoid system is a key neuromodulatory system. Fatty acid amide hydrolase, a key membrane-bound homodimeric degrading enzyme that regulates the biological activity of N-arachidonoylethanolamide in the eCB system and other essential bioactive lipids, is a key membrane-bound homodimeric degrading enzyme that regulates the biological activity of N-arachidonoylethanolamide in the eCB system and other important bioactive lipids. Although the results of these studies were mixed, the FAAH C385A genotype can influence susceptibility to certain multifactorial disorders and can be a potential therapeutic target.
Source link: https://europepmc.org/article/MED/36300805
Ischemic cardiomyopathy leads to inflammation and left ventricular dysfunction, causing left-ventricular dysfunction and left ventricular dysfunction. With worsened LV function in ischemic cardiomyopathy, Cannabinoid type-2 receptor deficiency leading to increased apoptosis and infarctions. Consequently, fatty acid amide hydrolase ineffective mice deficient -/- mice were subjected to repeated, daily 15 min, left anterior descending artery occlusion for three and seven days in a row. 00b1 agonist GW6471 i. v. as endocannabinoids also induce PPAR-u03b1-mediated effects of AEA, as endocannabinoids also stimulated PPAR-u03b1 mediated effects of AEA, according to PPAR-u03b1 antagonist GW6471 i. v. Taqman RT-qPCR and immune cells were analyzed by fluorescence-activated cell sorting using fluorescence-activated cell sorting. When FAAH -/- mice were treated with GW6471, collagen deposition was reduced to WT levels. Compared to WT, FAAH-/- mice's expression was markedly higher in FAAH -/- mice, followed by increased macrophage infiltration in infarcted regions, both being reversed by GW6471 therapy. We hypothesize that the rise in endocannabinoids may have partially detrimental effects on cardiomyocyte survival due to PPAR-u03b1 activation.
Source link: https://europepmc.org/article/MED/36293543
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