High-Mobility Group Box 1 (HMGB1) Protein in Parkinson's Disease Research: A 10-Year Bibliometric Analysis DOI Creative Commons
Khairiah Razali, Wael Mohamed

Journal of Integrative Neuroscience, Journal Year: 2023, Volume and Issue: 22(4), P. 87 - 87

Published: July 4, 2023

Parkinson's disease (PD), the most prevalent motoric neurodegenerative disease, has been intensively studied to better comprehend its complicated pathogenesis. Chronic neuroinflammation is a major factor contributing development of PD. Reportedly, high-mobility group box 1 (HMGB1) protein capable mediating neuroinflammatory response. In this regard, knowledge mapping research linking HMGB1 PD necessary.Herein, we perform dynamic and longitudinal bibliometric analysis explore hotspots current trends HMGB1-related publications during past decade.All focusing on were retrieved from PubMed database using search terms "Parkinson's disease" "hmgb1". Using filters, only English articles published between 2011 2022 selected. The Bibliometrix Biblioshiny packages R software used conduct analysis.The filtered identified 47 (34 original 13 review articles), 2022. There was an increase trend in number published, with annual growth rate 19.35 percent. scientific collaboration field, United States lead, followed by China, Malaysia, Australia. Compared other countries, China had highest level area. Neuroinflammation, microglia, receptor for advanced glycation end-products (RAGE) represent top three frontiers research. According thematic evolution analysis, over last decade, PD, microglia addressed individually, however, since 2017, these topics frequently discussed within same cluster: neuroinflammation. Furthermore, HMGB1, domains co-occurred majority discussion.The link realized decade ago becomes increasingly important time. Our findings can aid scholars comprehending global context HMGB1/PD relationship provide significant insights future

Language: Английский

Pain in rheumatoid arthritis: Emerging role of high mobility group box 1 protein-HMGB1 DOI

Anithakumari Aswathy Krishna,

Beena Levakumar Abhirami,

Alaganandam Kumaran

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: 362, P. 123361 - 123361

Published: Jan. 4, 2025

Language: Английский

Citations

1
High Mobility Group Box Protein (HMGB1): A Potential Therapeutic Target for Diabetic Encephalopathy DOI
Udit Kumar Dash, Debashree Mazumdar, Santosh Singh

et al.

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(10), P. 8188 - 8205

Published: March 13, 2024

Language: Английский

Citations

7
Is Drp1 a link between mitochondrial dysfunction and inflammation in Alzheimer’s disease? DOI Creative Commons

Oualid Sbai,

Veronica Bazzani,

Shreya Tapaswi

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2023, Volume and Issue: 16

Published: May 12, 2023

Recent advances highlight that inflammation is critical to Alzheimer Disease (AD) pathogenesis. Indeed, several diseases characterized by are considered risk factors for AD, such as type 2 diabetes, obesity, hypertension, and traumatic brain injury. Moreover, allelic variations in genes involved the inflammatory cascade AD. AD also mitochondrial dysfunction, which affects energy homeostasis of brain. The role dysfunction has been mostly neuronal cells. However, recent data demonstrating occurs cells, promoting secretion pro-inflammatory cytokines, turn induce neurodegeneration. In this review, we summarize finding supporting hypothesis inflammatory-amyloid describe demonstrate link between altered cascade. We focus summarizing Drp1, fission, showing Drp1 activation leads NLRP3 inflammasome, cascade, aggravates Amyloid beta (Ab) deposition tau-induced neurodegeneration, relevance pathway an early event

Language: Английский

Citations

11
Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer’s, Parkinson’s, and ALS DOI Open Access
Corneliu Toader,

Călin Petru Tătaru,

Octavian Munteanu

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12613 - 12613

Published: Nov. 24, 2024

Neurodegenerative diseases, such as Alzheimer's, Parkinson's, ALS, and Huntington's, remain formidable challenges in medicine, with their relentless progression limited therapeutic options. These diseases arise from a web of molecular disturbances-misfolded proteins, chronic neuroinflammation, mitochondrial dysfunction, genetic mutations-that slowly dismantle neuronal integrity. Yet, recent scientific breakthroughs are opening new paths to intervene these once-intractable conditions. This review synthesizes the latest insights into underlying dynamics neurodegeneration, revealing how intertwined pathways drive course diseases. With an eye on most promising advances, we explore innovative therapies emerging cutting-edge research: nanotechnology-based drug delivery systems capable navigating blood-brain barrier, gene-editing tools like CRISPR designed correct harmful variants, stem cell strategies that not only replace lost neurons but foster neuroprotective environments. Pharmacogenomics is reshaping treatment personalization, enabling tailored align individual profiles, while diagnostics biomarkers ushering era early, precise disease detection. Furthermore, novel perspectives gut-brain axis sparking interest mounting evidence suggests microbiome modulation may play role reducing neuroinflammatory responses linked neurodegenerative progression. Taken together, advances signal shift toward comprehensive, personalized approach could transform care. By integrating techniques, this offers forward-looking perspective future where treatments aim just manage symptoms fundamentally alter progression, presenting renewed hope for improved patient outcomes.

Language: Английский

Citations

4
HMGB1 blood levels and neurological outcomes after traumatic brain injury: Insights from an exploratory study DOI Creative Commons
Irma Wati Ngadimon, Devi Mohan, Mohd. Farooq Shaikh

et al.

Epilepsia Open, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 12, 2025

Abstract Objective Posttraumatic epilepsy (PTE) and cognitive impairment are severe complications following traumatic brain injury (TBI). Neuroinflammation likely contributes, but the role of specific inflammatory mediators requires clarification. High‐mobility group box 1 (HMGB1) is an cytokine released after that may be involved. This prospective longitudinal study investigated whether serum HMGB1 levels associated with PTE development decline over 12 months post‐TBI. Methods Serum samples were collected from 41 TBI patients, including mild moderate to severe, at baseline, 6, TBI. was quantified by ELISA alongside interleukin‐1β (IL‐1β) tumor necrosis factor (TNF). Cognitive assessments using validated neuropsychological performed 6 months. The occurrence also tracked. Results remained elevated post‐TBI only in subgroup ( n = 6) developed p 0.026). cases. Higher correlated a greater Addenbrooke's Examination scores < 0.05). Reductions 0.05), IL‐1β 0.05) TNF 0.001) improvements scores. Multivariate regression analysis confirmed level changes independently trajectory 0.003). Significance highlights importance understanding interactions between markers posttraumatic neuroinflammatory responses. Targeting offer promising strategy for managing chronic neuroinflammation mitigating deficits emphasizing potential targeted therapeutic interventions this context. Plain Language Summary examines how protein called contribute Patients higher more develop experience significant within year. Reducing related inflammation better function overall health. These findings suggest could valuable marker target treatments prevent improve recovery

Language: Английский

Citations

0
Oligodendrocyte Precursor Cell-Specific HMGB1 Knockout Reduces Immune Cell Infiltration and Demyelination in Experimental Autoimmune Encephalomyelitis Models DOI

Gil‐Ran Kim,

Jihye Seo, Bokyung Kim

et al.

Neuroscience Bulletin, Journal Year: 2025, Volume and Issue: unknown

Published: March 20, 2025

Language: Английский

Citations

0
Inhibition of FOXD3 O-GlcNAc Modification Ameliorates Spinal Cord Injury by Promoting STUB1-Mediated Ubiquitination Degradation of HMGB1 DOI
Wu Zhou, Bo Hei, Yihao Liu

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: April 24, 2025

Language: Английский

Citations

0
Plasma Concentrations of High Mobility Group Box 1 Proteins and Soluble Receptors for Advanced Glycation End-Products Are Relevant Biomarkers of Cognitive Impairment in Alcohol Use Disorder: A Pilot Study DOI Creative Commons
Fernando Rodrı́guez de Fonseca, Francisco Medina-Paz, Mira Sapozhnikov

et al.

Toxics, Journal Year: 2024, Volume and Issue: 12(3), P. 190 - 190

Published: Feb. 29, 2024

Alcohol use disorder (AUD) is a major component in the etiology of cognitive decline and dementia. Underlying mechanisms by which long-term alcohol abuse causes dysfunction include excessive oxidative stress inflammation brain, activated increased reactive oxygen/nitrogen species (ROS/RNS), advanced glycation end-products (AGEs) high-mobility group box 1 protein (HMGB1). In pilot study, we examine potential clinical value circulating biomarkers including ROS/RNS, HMGB1, soluble receptor for AGE (sRAGE), brain biomarker aging apolipoprotein D (ApoD), antioxidant regulator nuclear factor erythroid 2-related 2 (NRF2) as predictive indices impairment (CI) abstinent patients with AUD (n = 25) compared to established Alzheimer’s disease (AD, n 26) control subjects 25). Plasma concentrations sRAGE were evaluated immunoblotting; ROS/RNS fluorometric kit; ApoD, NRF2 ELISA. Abstinent had higher sRAGE, (p < 0.05), ApoD 0.01) concentrations, similar those AD patients, lower controls. These changes remarkable CI. correlated positively duration (rho 0.398, p 0.022; rho 0.404, 0.018), whereas negatively periods abstinence −0.340, 0.045). A model duration, was able differentiate CI (92.3% correct predictions, ROC-AUC= 0.90) from without conclusion, propose capable predicting patients.

Language: Английский

Citations

3
A multifunctional nanoplatform with dual-targeted antibacterial and cascaded immunomodulatory strategy for the treatment of bacterial keratitis DOI

Ruixiao Wang,

Yanhong Dong,

Jiteng Zhang

et al.

Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: 498, P. 155323 - 155323

Published: Aug. 30, 2024

Language: Английский

Citations

3
The HMGB1–RAGE axis in nucleus accumbens facilitates cocaine‐induced conditioned place preference via modulating microglial activation DOI Creative Commons
Jian Ye, Shuang‐Qi Gao,

Zi‐Cun Liu

et al.

Brain and Behavior, Journal Year: 2024, Volume and Issue: 14(3)

Published: March 1, 2024

Abstract Introduction Repeated exposure to cocaine induces microglial activation. Cocaine also a release of high mobility group box‐1 (HMGB1) from neurons into the extracellular space in nucleus accumbens (NAc). HMGB1 is an important late inflammatory mediator However, whether secretion acts on microglia or contributes addiction largely unknown. Methods Rats were trained by intraperitoneal administration and cocaine‐induced conditioned place preference (CPP). Expression was regulated viral vectors. Activation inhibited minocycline. Interaction receptor for advanced glycation end products (RAGE) disrupted peptide. Results injection facilitated signaling, together with delayed activation concurrently NAc. Furthermore, inhibition attenuated CPP. Box A, specific antagonist interrupt interaction RAGE, abolished expression reward memory. Meanwhile, HMGB1–RAGE suppressed activation, as well consolidation Conclusion All above results suggest that neural through which These findings offer axis new target treatment drug addiction.

Language: Английский

Citations

2