Article
Biochemistry & Molecular Biology
Zhi Ruan, Qing Lu, Jennifer E. Wang, Mi Zhou, Shuiqiao Liu, Hongxia Zhang, Akshay Durvasula, Yijie Wang, Yanan Wang, Weibo Luo, Yingfei Wang
Summary: The study found that MIF mediates TBI-induced neurodegeneration, neuronal cell death, and neurobehavioral dysfunction through its nuclease activity, but not its pro-inflammatory role. Targeting MIF's nuclease activity may offer a novel strategy to protect neurons from TBI.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2022)
Review
Multidisciplinary Sciences
Xinli Hu, Yu Xu, Haojie Zhang, Yao Li, Xiangyang Wang, Cong Xu, Wenfei Ni, Kailiang Zhou
Summary: This review summarizes the role of necroptosis in central nervous system trauma and its therapeutic implications, providing important suggestions for researchers conducting in-depth research. The study focuses on the necroptosis signaling pathway, execution, temporal patterns of RIPKs in CNS trauma, association of miRNAs with necroptosis, and different types of CNS trauma cell death. It also highlights potential agents for curtailing necroptosis-related cell death in CNS trauma.
JOURNAL OF ADVANCED RESEARCH
(2022)
Article
Multidisciplinary Sciences
Adam Z. Spitz, Emmanouil Zacharioudakis, Denis E. Reyna, Thomas P. Garner, Evripidis Gavathiotis
Summary: The BCL-2 family protein BAX plays a crucial role in regulating mitochondria-driven cell death, with the potential for aberrant cell death in diseases when dysregulated. The FDA-approved drug Eltrombopag is shown to directly inhibit BAX by preventing its conformational transformation and stabilizing its inactive structure, thereby inhibiting BAX-mediated apoptosis induced by cytotoxic stimuli.
NATURE COMMUNICATIONS
(2021)
Article
Neurosciences
Xingyun Quan, Li Song, Xiaomei Zheng, Shenjie Liu, Huaqiang Ding, Sijing Li, Guanghui Xu, Xin Li, Liang Liu
Summary: Studies have shown that alterations in autophagy-related proteins are extensive after traumatic brain injury (TBI), with controversy over whether TBI enhances or suppresses autophagy. Experimental findings revealed a significant increase in the levels of LC3-II and SQSTM1 proteins in the injured cortex group, suggesting accumulation of autophagosomes after TBI, while the specific autophagy inhibitor SAR405 reduced TBI-induced apoptosis and functional deficits.
Article
Immunology
Huayang Wang, Qibing Huang, Zhijie Zhang, Jian Ji, Tao Sun, Donghai Wang
Summary: The study found that CXCR2 is transiently overexpressed in peripheral monocytes of TBI patients post-surgery, which is associated with unfavorable outcomes. Serum and CSF from TBI patients promote CXCR2 expression in monocytes, and CXCR2 antagonist can decrease monocyte chemotaxis.
JOURNAL OF NEUROINFLAMMATION
(2022)
Article
Biochemistry & Molecular Biology
Si Hyun Lee, A. Ra Kho, Song Hee Lee, Dae Ki Hong, Beom Seok Kang, Min Kyu Park, Chang Juhn Lee, Hyun Wook Yang, Seo Young Woo, Se Wan Park, Dong Yeon Kim, Bo Young Choi, Sang Won Suh
Summary: Traumatic brain injury (TBI) leads to the aggravation of pre-existing brain dysfunction and promotes neurotoxic cascades. In this study, the researchers hypothesized that inhibition of the enzyme ASMase could reduce ceramide formation and prevent TBI-induced neuronal death. The results confirmed that the ASMase inhibitor, imipramine, effectively reduced ceramide production, oxidative stress, and neuronal death in a rat model of TBI, suggesting ASMase inhibition as a potential therapeutic strategy for reducing hippocampal neuronal death after TBI.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Neurosciences
Dengfeng Lu, Yi Wang, Guangjie Liu, Shixin Wang, Aojie Duan, Zongqi Wang, Jing Wang, Xiaoou Sun, Yu Wu, Zhong Wang
Summary: The expression of Armcx1 decreases and miR-223-3p levels increase in neurons after traumatic brain injury (TBI). Upregulation of Armcx1 alleviates TBI-induced neurological dysfunction, neuronal cell death, mitochondrial dysfunction, and axonal injury, while downregulation of Armcx1 has the opposite effect.
NEUROBIOLOGY OF DISEASE
(2023)
Review
Cell Biology
Xinli Hu, Yu Xu, Hui Xu, Chenqiang Jin, Haojie Zhang, Haohan Su, Yao Li, Kailiang Zhou, Wenfei Ni
Summary: Ferroptosis, a novel type of programmed cell death, has been found to be associated with acute central nervous system (CNS) trauma. The processes that induce ferroptosis include iron overload, imbalanced glutathione metabolism, and lipid peroxidation. Understanding the mechanism of ferroptosis is important for studying the pathophysiological process of CNS trauma.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Immunology
Yin Yuxiong, Xiang Xujin, Tang Yi, Chen Ya, Li Yujuan, Hu Shanshan, Wang Huiwen
Summary: Neuronal death and neuroinflammation are important factors in the progression of traumatic brain injury (TBI). This study reveals that a protein called TRAF7 plays a critical role in TBI by regulating cell death and inflammation. The interaction between TRAF7 and MEKK3 is a key step in the development of TBI, suggesting that TRAF7 could be a potential therapeutic target for TBI treatment.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Neurosciences
Jianhang Peng, Cheng Gao, Xueshi Chen, Tao Wang, Chengliang Luo, Mingyang Zhang, Xiping Chen, Luyang Tao
Summary: Traumatic brain injury (TBI) is a major cause of death and disability worldwide, with no specific drug treatment available. Previous studies have shown the neuroprotective effect of Ruxolitinib (Ruxo) on TBI, but further research is needed to understand the underlying mechanisms and potential clinical applications. This study used a mouse model of moderate TBI and found that Ruxo improved neurological deficits, reduced lesion volume, and maintained the homeostasis of CTSB, suggesting its potential as a therapeutic candidate for TBI.
EXPERIMENTAL NEUROLOGY
(2023)
Editorial Material
Cell Biology
Haibo Dong, Wei Guo, Zhanxiang Zhou
Summary: Lipotoxicity-induced lysosomal membrane permeabilization plays a role in the pathogenesis of alcohol-associated liver disease through the activation of BAX/MLKL signaling pathway.
Review
Cell & Tissue Engineering
Lin Zhong, Jingjing Wang, Peng Wang, Xiaoyin Liu, Peng Liu, Xu Cheng, Lujia Cao, Hongwei Wu, Jing Chen, Liangxue Zhou
Summary: Regenerative repair of the brain after traumatic brain injury remains a clinical challenge, and exosome therapy presents a promising strategy for novel regenerative therapies. Prior research has shown that exosomes produced by neural stem cells can participate in the physiological and pathological changes associated with TBI and have potential neuroregulatory and repair functions.
STEM CELL RESEARCH & THERAPY
(2023)
Article
Chemistry, Multidisciplinary
Zhiqiang Liu, Xiaowen Xing, Pengchong Zhu, Cui Wang, Mengwen Song, Lei Zhang, Xiaoming Zhu, Bin Ning, Yuming Fu, Zengqiang Yuan
Summary: In this study, it was discovered that hyaluronic acid (HA) can inhibit ferroptosis in acute traumatic brain injury (TBI) through receptor-mediated intrinsic signaling pathways. The upregulation of CD44 in the focus area of TBI was demonstrated, and the injection of HA nanoconjugates effectively reduced brain damage and behavioral defects. The study revealed the extracellular regulation of ferroptosis and contributed to the development of novel nanomaterials or nanodrugs for ferroptosis-related tissue injuries.
Review
Biochemistry & Molecular Biology
Mia C. Borlongan, Susanna Rosi
Summary: Traumatic brain injury (TBI) is a major cause of long-term neurological disabilities worldwide. It affects both soldiers and civilians and is characterized by inflammation in the brain. There are currently no treatments available to prevent or reverse the harmful effects of TBI. However, stem cell-based therapies hold promise for the treatment of TBI.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Neurosciences
Francesca Pischiutta, Enrico Caruso, Helena Cavaleiro, Antonio J. Salgado, David J. Loane, Elisa R. Zanier
Summary: Traumatic brain injury (TBI) patients require better neuroprotective/neuroreparative strategies. Mesenchymal stromal cells (MSCs) have shown promise in neuroprotection through paracrine mechanisms. Immunomodulation by MSC-derived secretome is a key mechanism for their therapeutic effects. Secretome promotes tissue repair and neurological recovery, but excessive neuroinflammatory response can worsen TBI.
EXPERIMENTAL NEUROLOGY
(2022)
Article
Neurosciences
Jianhua Peng, Yue Wu, Jinwei Pang, Xiaochuan Sun, Ligang Chen, Yue Chen, Jiping Tang, John H. Zhang, Yong Jiang
Article
Cell & Tissue Engineering
Cheng Yin, Zong-duo Guo, Zong-ze He, Zhen-yu Wang, Xiao-chuan Sung
CELL TRANSPLANTATION
(2019)
Article
Clinical Neurology
Jianfeng Zheng, Rui Xu, Zongduo Guo, Xiaochuan Sun
CURRENT NEUROVASCULAR RESEARCH
(2019)
Article
Neurosciences
Zhihao Chen, Hong Wang, Jianjun Zhong, Junqing Yang, Rami Darwazeh, Xiaocui Tian, Zhijian Huang, Li Jiang, Chongjie Cheng, Yue Wu, Zongduo Guo, Xiaochuan Sun
EXPERIMENTAL NEUROLOGY
(2019)
Article
Neurosciences
Liu Liu, Ping Zhang, Zhaosi Zhang, Qin Hu, Junchi He, Han Liu, Jun Zhao, Yidan Liang, Zhaohui He, Xinghua Li, Xiaochuan Sun, Zongduo Guo
Article
Clinical Neurology
Jianfeng Zheng, Zongduo Guo, Rui Xu, Zhaohui He, Xiaochuan Sun
WORLD NEUROSURGERY
(2019)
Article
Neurosciences
Liang Wang, Zhaosi Zhang, Luodan Liang, Yue Wu, Jianjun Zhong, Xiaochuan Sun
NEUROSCIENCE LETTERS
(2019)
Article
Clinical Neurology
Shengxi Wang, Zhijian Huang, Rui Xu, Zhengbu Liao, Yi Yan, Wenyuan Tang, Yongzhi Xia
WORLD NEUROSURGERY
(2020)
Article
Oncology
Zhaohua Tang, Gang Yang, Xiaoshu Wang, Feilan Chen, Zhengbu Liao, Zhiwei Zhang, Zili Liu, Wenxin Zeng, Min Fang, Wentao Wang, Xiaochuan Sun, Gang Huo
JOURNAL OF NEURO-ONCOLOGY
(2020)
Article
Pharmacology & Pharmacy
Chongjie Cheng, Xiaoshu Wang, Yinghua Jiang, Yadan Li, Zhengbu Liao, Wenlu Li, Zhanyang Yu, Michael J. Whalen, Josephine Lok, Aaron S. Dumont, Ning Liu, Xiaoying Wang
Summary: Microvascular failure is crucial in the pathological evolution after TBI. Annexin A2 has shown potential in protecting against cerebral permeability and angiogenesis impairment, suggesting it as a candidate for cerebrovascular therapy. In experiments, rA2 treatment improved BBB integrity, enhanced mRNA levels of pro-angiogenic factors, activated cellular signaling pathways, induced angiogenesis, and improved long-term neurological function after TBI.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Chenrui Wu, Mengran Du, Renqiang Yu, Yuqi Cheng, Biying Wu, Jiayuanyuan Fu, Weilin Tan, Qiang Zhou, Ehab Balawi, Z. B. Liao
Summary: The study found that melatonin could alleviate ferroptosis and endoplasmic reticulum stress after traumatic brain injury by regulating the circPtpn14/miR-351-5p/5-LOX signaling pathway, providing evidence for its anti-ferroptotic and anti-ER stress effects in brain injury.
FREE RADICAL BIOLOGY AND MEDICINE
(2022)
Article
Cell Biology
Yu-Qi Cheng, Chen-Rui Wu, Meng-Ran Du, Qiang Zhou, Bi-Ying Wu, Jia-Yuan-Yuan Fu, Ehab Balawi, Wei-Lin Tan, Zheng-Bu Liao
Summary: In this study, the researchers found that circLphn3 expression was decreased in traumatic brain injury models and hemin-treated bEnd.3 cells. They also discovered that circLphn3 acted as a molecular sponge for miR-185-5p and regulated the expression of tight junction proteins, improving the permeability of the blood-brain barrier.
NEURAL REGENERATION RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Mengran Du, Chenrui Wu, Renqiang Yu, Yuqi Cheng, Zhaohua Tang, Biying Wu, Jiayuanyuan Fu, Weilin Tan, Qiang Zhou, Ziyu Zhu, Ehab Balawi, Xuekang Huang, Jun Ma, Z. B. Liao
Summary: This study investigated the expression of circRNAs and their relation with neurological dysfunction after TBI. The research found that circIgfbp2 was significantly increased in injured brain tissue and in TBI patients, and its levels were positively correlated with anxiety symptoms. Knockdown of circIgfbp2 relieved anxiety-like behaviors and sleep disturbances induced by TBI. Mechanistically, circIgfbp2 targeted miR-370-3p to regulate BACH1, and down-regulating BACH1 alleviated mitochondrial dysfunction and oxidative stress-induced synapse dysfunction. Therefore, circIgfbp2 may be a novel therapeutic target for anxiety and sleep disorders after TBI.
MOLECULAR PSYCHIATRY
(2022)
Article
Neurosciences
Jiayuanyuan Fu, Qiang Zhou, Biying Wu, Xuekang Huang, Zhaohua Tang, Weilin Tan, Ziyu Zhu, Mengran Du, Chenrui Wu, Jun Ma, Ehab Balawi, Z. B. Liao
Summary: This study investigated the protective effect and regulatory pathways of melatonin in a traumatic brain injury (TBI) mice model using transcriptomics and bioinformatics analysis. The results showed differential expression profiles of mRNA, lncRNA, miRNA, and circRNA after melatonin treatment. The study also revealed the regulatory relationship between non-coding RNAs and mRNA in TBI treatment. Furthermore, the expression changes of key genes in the synaptic vesicle cycle pathway were validated after melatonin treatment. Overall, this research provides new insights into the molecular effect of melatonin in TBI treatment.
FRONTIERS IN MOLECULAR NEUROSCIENCE
(2022)
Article
Clinical Neurology
Yue Wu, Qiuguang He, Yuling Wei, Ji Zhu, Zhaohui He, Xiaodong Zhang, Zongduo Guo, Rui Xu, Chongjie Cheng, Zhijian Huang, Xiaochuan Sun
NEUROPSYCHIATRIC DISEASE AND TREATMENT
(2019)
