Please use this identifier to cite or link to this item: http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/5188
Title: The Role of Neuroinflammatory Mediators in the Pathogenesis of Traumatic Brain Injury: A Narrative Review
Authors: Doganyigit, Zuleyha
Erbakan, Kaan
Akyuz, Enes
Polat, Ayse Kristina
Arulsamy, Alina
Shaikh, Mohd Farooq
Ordu Üniversitesi
0000-0002-5581-500X
0000-0001-9865-6224
Keywords: Cytokines, neuroinflammation, brain injury, glia, interleukin
GROWTH-FACTOR-BETA, IL-2 RECEPTOR, BIOMARKER, MODEL, PATHOPHYSIOLOGY, INTERLEUKIN-2, INVOLVEMENT, DYSFUNCTION, EXPRESSION, TOLERANCE
Issue Date: 2022
Publisher: AMER CHEMICAL SOC-WASHINGTON
Citation: Doganyigit, Z., Erbakan, K., Akyuz, E., Polat, AK., Arulsamy, A., Shaikh, MF. (2022). The Role of Neuroinflammatory Mediators in the Pathogenesis of Traumatic Brain Injury: A Narrative Review. ACS Chem. Neurosci.. https://doi.org/10.1021/acschemneuro.2c00196
Abstract: Traumatic brain injury (TBI) is a debilitating acquired neurological disorder that afflicts nearly 74 million people worldwide annually. TBI has been classified as more than just a single insult because of its associated risk toward various long-term neurological and neurodegenerative disorders. This risk may be triggered by a series of postinjury secondary molecular and cellular pathology, which may be dependent on the severity of the TBI. Among the secondary injury mechanisms, neuroinflammation may be the most crucial as it may exacerbate brain damage and lead to fatal consequences when prolonged. This Review aimed to elucidate the influence of neuroinflammatory mediators on the TBI functional and pathological outcomes, particularly focusing on inflammatory cytokines which were associated with neuronal dysfunctions in the acute and chronic stages of TBI. These cytokines include interleukins (IL) such as IL-1(beta)beta, IL-4, IL-6, IL8, IL-10, IL-18, IL-33 and tumor necrosis factor alpha (TNF-alpha), which have been extensively studied. Apart from these, IL-2, interferon gamma (IFN-gamma), and transforming growth factor-beta (TGF-beta) may also play a significant role in the pathogenesis of TBI. These neuroinflammatory mediators may trigger a series of pathological events such as cell death, microglial suppression, and increased catecholaminergic activity. Interestingly, in the acute phase of TBI, most of these mediators may also play a neuroprotective role by displaying anti-inflammatory properties, which may convert to a pro-inflammatory action in the chronic stages post TBI. Early identification and treatment of these mediators may help the development of more effective treatment options for TBI.
Description: WoS Categories: Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
Web of Science Index: Science Citation Index Expanded (SCI-EXPANDED)
Research Areas: Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences & Neurology
URI: http://dx.doi.org/10.1021/acschemneuro.2c00196
https://www.webofscience.com/wos/woscc/full-record/WOS:000819851900001
http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/5188
ISSN: 1948-7193
Appears in Collections:Dahili Tıp Bilimleri

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