Cited by 311Advanced Glycation End Products researchNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular Disturbances

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HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

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Paudel, Yam Nath, Shaikh, Mohd. Farooq, Chakraborti, Ayanabha, Kumari, Yatinesh, Aledo-Serrano, Ángel, Aleksovska, Katina, Alvim, Marina Koutsodontis Machado, Othman, Iekhsan·2018·Frontiers in Neuroscience

DOI 10.3389/fnins.2018.00628PMC PMC6142787

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Abstract

High mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein released by glia and neurons upon inflammasome activation and activates receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR) 4 on the target cells. HMGB1/TLR4 axis is a key initiator of neuroinflammation. In recent days, more attention has been paid to HMGB1 due to its contribution in traumatic brain injury (TBI), neuroinflammatory conditions, epileptogenesis, and cognitive impairments and has emerged as a novel target for those conditions. Nevertheless, HMGB1 has not been portrayed as a common prognostic biomarker for these HMGB1 mediated pathologies. The current review discusses the contribution of HMGB1/TLR4/RAGE signaling in several brain injury, neuroinflammation mediated disorders, epileptogenesis and cognitive dysfunctions and in the light of available evidence, argued the possibilities of HMGB1 as a common viable biomarker of the above mentioned neurological dysfunctions. Furthermore, the review also addresses the result of preclinical studies focused on HMGB1 targeted therapy by the HMGB1 antagonist in several ranges of HMGB1 mediated conditions and noted an encouraging result. These findings suggest HMGB1 as a potential candidate to be a common biomarker of TBI, neuroinflammation, epileptogenesis, and cognitive dysfunctions which can be used for early prediction and progression of those neurological diseases. Future study should explore toward the translational implication of HMGB1 which can open the windows of opportunities for the development of innovative therapeutics that could prevent several associated HMGB1 mediated pathologies discussed herein.

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Additional file 1 of Vesicular HMGB1 release from neurons stressed with spreading depolarization enables confined inflammatory signaling to astrocytes
Kaya, Ζ., Belder, N., Sever, M., Dönmez‐Demir, B., Erdener, Ş. E., Bozbeyoglu, N., Bagci, C., Eren‐Koçak, E., Yemişçi, M., Karataş, H., et al. (2023) · Figshare · doi:10.6084/m9.figshare.24792331
Additional file 4 of Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury
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Additional file 2 of Vesicular HMGB1 release from neurons stressed with spreading depolarization enables confined inflammatory signaling to astrocytes
Kaya, Ζ., Belder, N., Sever, M., Dönmez‐Demir, B., Erdener, Ş. E., Bozbeyoglu, N., Bagci, C., Eren‐Koçak, E., Yemişçi, M., Karataş, H., et al. (2024) · Figshare · doi:10.6084/m9.figshare.24792405
Additional file 3 of Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury
Fan, H., Tang, H.-B., Chen, Z., Wang, H.-Q., Zhang, L., Jiang, Y., Li, T., Yang, C.-F., Wang, X., Li, X., et al. (2020) · Figshare · doi:10.6084/m9.figshare.13076609
Additional file 2 of Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury
Fan, H., Tang, H.-B., Chen, Z., Wang, H.-Q., Zhang, L., Jiang, Y., Li, T., Yang, C.-F., Wang, X., Li, X., et al. (2020) · Figshare · doi:10.6084/m9.figshare.13076606
Additional file 1 of Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury
Fan, H., Tang, H.-B., Chen, Z., Wang, H.-Q., Zhang, L., Jiang, Y., Li, T., Yang, C.-F., Wang, X., Li, X., et al. (2020) · Figshare · doi:10.6084/m9.figshare.13076603
Additional file 1 of Pregabalin mitigates microglial activation and neuronal injury by inhibiting HMGB1 signaling pathway in radiation-induced brain injury
Zhang, Z., Jiang, J., He, Y., Cai, J., Xie, J., Wu, M., Xing, M., Zhang, Z., Chang, H., Yu, P., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21184231
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Authors: Paudel, Y. N., Shaikh, M. F., Chakraborti, A., Kumari, Y., Aledo-Serrano, Á., Aleksovska, K., Alvim, M. K. M., & Othman, I.
Affiliations: Monash University Malaysia (MY)
University of Alabama at Birmingham (US)
Ss. Cyril and Methodius University in Skopje (MK)
Universidade Estadual de Campinas (UNICAMP) (BR)
Corresponding author: Shaikh, Mohd. Farooq
ORCID: Paudel, Yam Nath
Shaikh, Mohd. Farooq
Chakraborti, Ayanabha
Kumari, Yatinesh
Aleksovska, Katina
Alvim, Marina Koutsodontis Machado
Othman, Iekhsan
Venue: Frontiers in Neuroscience
Publisher: Frontiers Media SA
Published: 2018-09-11
Volume: 12
Pages: 628-628
ISSN: 1662-453X (ISSN-L)
DOI: 10.3389/fnins.2018.00628
PMC: PMC6142787
OpenAlex: W2889849480
Cited by: 311
References: 166
Citations by year: 2026: 38 · 2025: 29 · 2024: 36 · 2023: 33 · 2022: 56 · 2021: 45 · 2020: 53 · 2019: 19 · 2018: 2
FWCI: 3.87
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: Frontiers in Neuroscience (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Monash University Research Portal (Monash University) (submittedVersion, cc-by)
Charles Sturt University Research Output (CRO) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Monash University
Monash University Malaysia
Jaypee University of Information Technology
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords: HMGB1, traumatic brain injury, neuroinflammation, epileptogenesis, cognitive impairment, TLR4, RAGE, inflammasome, prognostic factors, neuroinflammatory disorders

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HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

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