In the present day, more than 38% of the adult population can be considered overweight. The number has doubled in the past few decades. As the burden of metabolic diseases rise and Man himself acts as the agent of the disease, obesity precipitates several complications- the cardiac ones being significant. Obesity thus remains an important factor for Myocardial infarction. Myocardial infarction due to decreased blood supply often precipitates into heart failure. Nearly 25 percent of these patients with myocardial infarction develop heart failure within four years.
It is the death of the cells in the heart that should elicit inflammation. However, this mechanism of cell injury followed by inflammation is a highly censored phenomenon.
There are various mediators involved which again act on a variety of receptors.in the cell. One such is ALX/FRP2. This receptor has been recently found to act as a sensor for inflammation in myocardial infarction.
N-formyl peptide receptor 2 (FPR2) is located on the surface of many types of cells, especially immune cells. It regulates cell function by binding any one of a wide variety of molecules. These ligands include various peptides and metabolites of fatty acids, for example, lipoxin A4. It is due to this reason that the Receptor is known as ALX/FPR2 receptor.
Though earlier known to have been involved in bacterial killing and phagocytosis in response to its conventional ligand, N-formyl peptide, it also binds to Lipoxin A4 and Resolvin D1. It is the lipophilic property of the receptor that confers it the role it plays in inflammation.
Resolvins are metabolic byproducts of omega-3 fatty acids, primarily eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as well as docosapentaenoic acid (DPA) and clupanodonic acid.
Lipoxins, on the other hand, is Arachidonic acid metabolites.
As per recent studies, Resolvins inhibit the Leukotriene B4 receptor, a receptor for inflammation-promoting PUFA metabolites such as LTB4.
However, this lipoxins and Resolvin also lead to the development of obesity, cognitive decline, reproduction, neuroprotection, and cancer.
A recent experiment was performed at the University of Alabama at Birmingham (UAB)-the research team aimed to find out the effect of these molecules in mice.n the mouse experiments, Halade, the head researcher and colleagues boosted the amount of resolvin D1 by injection 3 hours after experimental myocardial infarction. A few similar mice were infected with normal saline.
The research paper states- ” Resolvin D1 reduces post-attack heart failure.”
A mechanism to has been proposed. Resolvins protected inside liposomes, had less left ventricle enlargement, and improved left ventricle function, less lung edema, and reduced collagen deposition, as compared with heart attack mice that received only saline.
They found that ALX/FPR2 was plentiful in these human ischemic hearts, and it was located in the cytoplasm of the myocardium cells.
Lipoxins play an important role by inhibiting leucocyte recruitment into the left ventricle from splenic reserves and promoting wound healing. After heart failure, these pro-resolving mediators decrease. Halade suggests that this is due to impaired cross-talk between the injured heart and splenic leukocytes.
While physicians mainly aim at reducing risk factors for the disease and rely on conventional drugs, this receptor serves as a therapeutic target in order to prevent the progress of the disease. A myriad of facts in this regard still lie unraveled.
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