Asuman Akkaya Fırat

By Asuman Akkaya Fırat

Ferroptosis is one of the forms of programmed cell death. Besides being a necessary micronutrient, iron is the key element that initiates ferroptosis in the cell. Intracellular unstable iron accumulation increases the amount of intracellular ROS, especially by the peroxidation of unsaturated membrane phospholipids. Insufficient antioxidant capacity and decreased glutathione levels play an important role in this process. The research reveals that an imbalance between unoxidized polyunsaturated fatty acids (PUFAs) and oxidized PUFAs, particularly oxidized arachidonic acid, accelerates ferroptosis. These oxidative reactions change the permeability of lysosomal and cellular membranes and cell death occurs. Iron chelators, lipophilic antioxidants, and specific inhibitors prevent ferroptosis. In addition to being accepted as a physiological process, it seems to be associated with tissue reperfusion damage, ischemic, neurodegenerative diseases, hematological and nephrological disorders. Ferroptosis is also being explored as a treatment option where it may offer a treatment option for some types of cancer. In this section, the brief history of ferroptosis, its morphological, molecular, and pathophysiological features are mentioned. Ferroptosis seems to be a rich field of research as a treatment option for many diseases in the future.

Part of the book: Iron Metabolism

By Asuman Akkaya Fırat

Chemokines or chemotactic cytokines are chemical signaling molecules that have a regulatory effect on the orientation of endothelial and epithelial cells, especially leukocytes, immune and inflammatory response, and cell regeneration. They are important in the management of endothelial damage, physical harm, atherosclerosis, vascular injury, bleeding, coagulation, interneuron transmission, and platelet functions. Chemokines are divided into four main subfamilies: CXC, CC, CX3C, and C. All of these proteins exert their biological effects by interacting with G-protein-coupled transmembrane receptors called chemokine receptors, which are selectively present on the surfaces of their target cells. Platelet chemokines increase the recruitment of various hematopoietic cells to the vascular wall by nurturing processes, such as neointima formation, atherosclerosis, and thrombosis, while also promoting vessel repair and regeneration after vascular injury. Regarding platelets, CXCL4 (platelet factor 4 and PF4) and the chemokine CXCL7, which is processed from platelet basic protein to connective tissue activating peptide-III and β-thrombomodulin, to its active form neutrophil-activating peptide-2, which are the most abundant. In this chapter, chemokines that are more effective on platelets will be discussed.

Part of the book: Chemokines Updates

By Asuman Akkaya Fırat

Eosinophils are white blood cells. They are found in various cellular arrays. Eosinophils play a role in the fight against many parasitic infections. Eosinophilic asthma, nasal polyps, eosinophilic gastrointestinal disorders, polyangiitis, and eosinophilic granulomatosis are diseases referring hypereosinophilic syndrome. Eosinophil granules participate in tissue healing, damage, repair and restructuring processes thanks to proteins and chemical mediators. Interleukin (IL)-5, IL-4, and IL-13′ play a role in the proliferation, maturation, activation, and recruitment of eosinophils. Eosinophils have receptors for various cytokines, chemokines, and adhesion molecules that allow them to participate in inflammatory activities. In response to stimuli, eosinophils may release a range of granule proteins, including major basic proteins (MBPs) 1–2, eosinophil cationic protein (ECP), eosinophil peroxidase (EPX), eosinophil-derived neurotoxin (EDN), cytokines, and cytosolic Charcot-Leyden crystal protein/ galectin-10 (CLC/Gal-10). Eosinophils participate in a variety of biological processes and contribute to both normal and pathological processes. Improvements can be made in understanding the pathophysiological mechanisms of these diseases. It has led to the development of new therapeutics for eosinophilic inflammatory diseases.

Part of the book: Eosinophils and Their Role in Human Health and Disease [Working title]