Dr. Kara completed her doctorate in the Department of Anatomy at the Faculty of Veterinary Medicine in 2017. She became an associate professor in 2022 and is currently working in the Faculty of Veterinary Medicine, Department of Anatomy, Atatürk University, Turkey. She has authored and co-authored nineteen journal papers, two book chapters, and thirty-two other types of publications.
Melatonin is an endocrine product released from the gland known as the pineal gland and is predominantly secreted during the night. Light exerts an inhibitory effect on melatonin secretion in the pineal gland. The suprachiasmatic nucleus controls pineal melatonin synthesis and its release via the peripheral sympathetic nervous system, which includes synapses in the intermediolateral cell column of the thoracic cord and its projection toward the superior cervical ganglia. Melatonin regulates many physiological functions in the body through membrane receptors and nuclear binding sites. In a chick study, the presence of melatonin receptors in cardiomyocytes was reported and, in another study, MT1 and MT2 membrane receptors were identified in left ventricular cardiomyocytes of the human heart. For this reason, it is suggested that melatonin has some regulatory effects on the cardiovascular system. Ischemic heart disease and myocardial infarctions are the main cause of cardiovascular death. Studies have shown that melatonin applications reduce the amount of blood cholesterol, LDL, and triglyceride and increase the amount of HDL. In light of these data, it can be said that melatonin is an important cardiovascular system protector. In this chapter, the protective effects and mechanisms of melatonin on the cardiovascular system will be discussed.
Part of the book: Melatonin
The endoplasmic reticulum (ER) is an organelle responsible for protein production in the cell and provides hemostasis in the cell. ER stress is stimulated by folded proteins, while the unfolded protein response (UPR) creates a response to ER stress and provides the cell survival. UPR modulation in mammals is provided with three major ER stress sensors, including transmembrane kinase 1, protein kinase-like ER kinase, and activating transcription factor 6. Because neurons are susceptible to misfolded proteins, severe or prolonged ER stress activates apoptotic cell death signals in the cell. Neurodegenerative diseases characterized by this condition are Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, characterized by the accumulation and aggregation of misfolded proteins. In addition, ER stress can lead to depression, schizophrenia, sleep disruption, and post-traumatic stress disorders. Neurons are highly susceptible to protein misfolding and apoptotic cell death. For this reason, UPR modulation contributes to preventing the neurodegenerative process in cells with misfolded protein folding. The relationship between ER stress, UPR, and neuropathology is significant for understanding this process. This section will discuss the effects of ER stress between UPR modulation and neurodegenerative disorders, and the histopathological changes in the mentioned neurodegenerative diseases will be mentioned.
Part of the book: Molecular Histopathology and Cytopathology