Turning stink into therapy for atherosclerosis

Turning stink into therapy for atherosclerosis

In an amusing but amazing turnaround, it seems the most foul-smelling compound on earth, called putrescine, could help relieve chronic inflammation, most importantly in the arterial thickening called atherosclerosis. This discovery is reported in the journal Cell Metabolism in January 2020. Putrescine Putrescine, spermine and spermidine are all organic compounds belonging to the polyamine class, and found widely within the human body, and in all animal meat, in fact. These seem to be vital ingredients for normal growth (“growth factors”) and are required for DNA regulation and protein synthesis. They also take up potentially damaging reactive oxygen species (ROS), and promote cell differentiation and proliferation, two processes vital in early embryonic life. Putrescine is also a by-product of bacterial breakdown of lysine and ornithine in the gut. The chemical putrescine takes its name from its stench – the unmistakable odour of rotting or putrid flesh. The current study was focused on how the body normally removes dead cells, using macrophages. Macrophages are white cells, phagocytes that move around looking for things to ‘eat’ and thus rid the body of unwanted matter like bacteria, debris from normal cell activity, and inflammatory by-products. The importance of efferocytosis Study author Ira Tabas says, “It's estimated that a billion cells die in the body every day, and if you don't get rid of them, they can cause inflammation and tissue death. Removing these dead cells by a process called 'efferocytosis' (from the Latin 'to carry to the grave') is one of the body's most important functions.” Apoptosis is the meticulously designed cell program in which the cell sets out to fade out of existence without causing harm to the rest of the body. The dead cell must be immediately removed by phagocytosis, or being engulfed by macrophages, to keep it from rotting and releasing cell debris which provoke inflammation. Autoantigens, or antigens belonging to the body’s own tissues but abnormally presented to the immune system as immune targets, perhaps because of their association with legitimate targets, could provoke autoimmune disease. In normal circumstances, this process of removing dying or dead cells begins almost as soon as the cell dies. On the other hand, in people with atherosclerosis and other chronic inflammatory conditions, efferocytosis appears to lag. This may be the trigger for the formation of the characteristic atherosclerotic plaques that narrow, stiffen and may finally obstruct the vessels, leading to serious and even fatal limitation of blood supply to the vital organs of the body. Closeup of a atherosclerosis- 3D rendering. Image Credit: Crevis / Shutterstock The study and its findings Related Stories



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