Abstract
Human red blood cells (RBCs), senescent or damaged due to particular stress, can be removed by programmed suicidal death, a process called eryptosis. There are various molecular mechanisms underlying eryptosis. The most frequent is the increase in the cytoplasmic concentration of Ca2+ ions, later exposure of erythrocytes to oxidative stress, hyperosmotic shock, ceramide formation, stimulation of caspases, and energy depletion. Phosphatidylserine (PS) exposed by eryptotic RBCs due to interaction with endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor, causes the RBCs to adhere to vascular wall with consequent damage to the microcirculation. Eryptosis can be triggered by various xenobiotics and endogenous molecules, such as high cholesterol levels. The possible diseases associated with eryptosis are various, including anemia, chronic kidney disease, liver failure, diabetes, hypertension, heart failure, thrombosis, obesity, metabolic syndrome, arthritis, and lupus. This review addresses and collates the existing ex vivo and animal studies on the inhibition of eryptosis by food-derived phytochemicals and natural compounds including phenolic compounds (PC), alkaloids, and other substances that could be a therapeutic and/or co-adjuvant option in eryptotic-driven disorders, especially if they are introduced through the diet.
Highlights
red blood cells (RBCs) due to interaction with endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor, causes the RBCs to adhere to vascular wall with consequent damage to the microcirculation
The hematopoietic processes mediated by the bone marrow and the hemocateretic processes mediated by macrophages that lead to the elimination of senescent or damaged RBCs, are in constant equilibrium
Clinicalto evidence suggests that eryptosis role in thethat development of all risk factors associated with metabolic bolic syndrome, aa key pathology involves a series of metabolic factors thatsyndrome, increasesuch risks as hyperglycemia, dyslipidemia, hypertension, and obesity, and clinical complications, of cardiovascular diseases, diabetes, and associated diseases, such as dementia [6]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. It was thought that because they lack a nucleus and mitochondria, RBCs were unable to undergo programmed cell death This hypothesis has been denied by much experimental evidences that has demonstrated the existence of the process known as eryptosis, which regulates the elimination of damaged or senescent RBCs [3]. The hematopoietic processes mediated by the bone marrow these processes can alter the number of circulating erythrocytes, compromising the oxygenation capacity of the tissues. The hematopoietic processes mediated by the bone marrow and the hemocateretic processes mediated by macrophages that lead to the elimination of senescent or damaged RBCs, are in constant equilibrium. This balance is finely regulated by erythropoietin [5]. Ca2+ channels, that allow extracellular Ca2+ to enters [6]
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