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Aging, neurogenesis and neuroinflammation in hearing loss and protection

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196449 Year: Pages: 151 DOI: 10.3389/978-2-88919-644-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-08-16 10:34:25
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Abstract

Worldwide, 278 million people are estimated to have moderate to profound hearing loss. Age-related hearing loss, also known as presbyacusis, affects approximately half of the population over 60 years old, making it the second most common cause of disability in older people. Hearing loss occurs when the sensory cells and neurons of the cochlea degenerate and die. The vestibular system, which holds the sense of balance, shares a common embryonic origin with the cochlea and together conform the inner ear. Balance problems are a trait of ageing to the point that balance ability is considered a sensor of physical decline and vestibular degeneration is the most common cause of falls in the elderly. Still the molecular bases of ageing in the vestibular system have not been studied in detail. Genetic and environmental factors contribute to the progression of age-related hearing loss (ARHL). Being noise the main environmental noxious agent for human hearing in the industrialized societies. There is no restorative treatment for deafness but functional replacement by means of prosthesis. Therefore, prevention and treatment of hearing loss is an unmet medical need. To develop innovative medical strategies against hearing loss, it is critical to understand the causes of ARHL and the essential pathways responsible for the manifestation of this complex disease. In this research topic, experts will discuss the stages and molecular elements of the damage and repair processes involved in ARHL, from cellular processes to molecules involved in aging. Oxidative stress takes a central stage as an essential element in the progression of injury and cell loss, and a target for cell protection strategies. Finally, the mechanisms of action and the potential of novel therapies for hair cell repair and protection will be discussed along with drug delivery strategies.

Peroxiredoxin 6 as a Unique Member of the Peroxiredoxin Family

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ISBN: 9783038979340 9783038979357 Year: Pages: 152 DOI: 10.3390/books978-3-03897-935-7 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Therapeutics
Added to DOAB on : 2019-06-26 08:44:06
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The peroxiredoxin family was discovered approximately 30 years ago and is now recognized as one of the most important families of enzymes related to antioxidant defense and cellular signaling. Peroxiredoxin 6 shares the basic enzymatic functions that characterize this family, but also exhibits several unique and crucial activities. These include the ability to reduce phospholipid hydroperoxides, phospholipase A2 activity, and an acyl transferase activity that is important in phospholipid remodeling. This book describes the available models for investigating the unique functions of PRDX6 and its role in normal physiological function, as well its roles in the pathophysiology of diseases including cancer, diseases of the eye, and male fertility.

Roles and Functions of ROS and RNS in Cellular Physiology and Pathology

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ISBN: 9783039287826 / 9783039287833 Year: Pages: 230 DOI: 10.3390/books978-3-03928-783-3 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Pathology
Added to DOAB on : 2020-06-09 16:38:57
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Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.

Keywords

human neuroblastoma SH-SY5Y cells --- TRPM2 channel --- ROS --- neuronal cell death --- histamine --- calcium --- endothelial cells --- NADPH-oxidase --- VAS2870 --- von Willebrand factor --- aorta --- relaxation --- reactive oxygen species (ROS) --- oxidative stress --- lipid peroxidation --- acrolein --- 4-hydroxynonenal (4-HNE) --- oxidative burst --- granulocytes --- cancer cells --- growth control --- cancer regression --- hydroxyapatite-based biomaterials --- osteoblast growth --- redox balance --- vitamins --- lipid peroxidation --- 4-hydroxynonenal --- oxidative stress --- oxidative stress --- nuclear factor erythroid 2–related factor 2 --- heme-oxygenase-1 --- macrophages --- plaque vulnerability --- optical coherence tomography --- reactive oxygen species --- free radicals --- DNA damage --- cyclopurines --- DNA and RNA polymerases --- nucleotide excision repair --- LC-MS/MS --- xeroderma pigmentosum --- cancer --- intermittent hypoxia --- mitochondria --- Ca2+, ROS --- antioxidant --- free radicals --- antimicrobial --- toll-like receptors --- cannabidiol --- UV radiation --- keratinocytes --- antioxidants --- inflammation --- intracellular signaling --- Nrf2 --- NF?B --- glucose deprivation --- glutamine deprivation --- viability --- proliferation --- ROS --- NRF2-NQO1 axis --- IMR-90 --- NQO1 transcript variants --- rs1800566 --- TP53 mutation --- oxidative stress --- MFN2 --- mitochondria --- fusion/fission --- oxidative stress --- blood–brain barrier --- bEnd5 --- bEnd.3 --- glutathione --- viability --- free radicals --- redox balance --- cell signaling --- growth --- toxicity --- antioxidants --- oxidative homeostasis --- oxidative metabolism of the cells --- pathophysiology of oxidative stress

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