摘要：
Diabetic nephropathy (DN) is one of the most serious and general complications of diabetes, while schedules for prevention and treatment are unsatisfactory. Leucine aminopeptidase (LAP) as one of the biomarkers of DN is associated with glomerular and/or tubular injury. Imaging of LAP activity in DN disease model in vivo is thus beneficial for early diagnosis and prevention of DN, but such a strategy is still lacking. Herein, an enzyme-activated probe HD-LAP with a NIR fluorescence emission for specific detection of LAP activity in the DN model is designed and synthesized. HD-LAP has a significant fluorescence enhancement after reacted with LAP and shows a NIR fluorescence emission at 704 nm based on intramolecular charge transfer mechanism. Moreover, HD-LAP can be employed to image LAP activity in HK-2 and HepG2 cells. More importantly, HD-LAP is the first example to real-time image LAP in DN mice and clinical serum samples. These results demonstrated that HD-LAP is promising as a powerful tool for the research on LAP associated diabetic diseases in future.
期刊：
FRONTIERS IN NEUROLOGY,2024年15:1322228 ISSN：1664-2295
通讯作者：
Zhu, Shuzhen;Wang, Q
作者机构：
[Zhu, Shuzhen; Li, Fangyi; Zhang, Wenjie; Deng, Bin; Zhu, SZ; Wang, Qing; Zhou, Hang; Wang, Q; Weng, Guomei; Luo, Yuqi] Southern Med Univ, Dept Neurol, Zhujiang Hosp, Guangzhou, Peoples R China.;[Li, Fangyi] Univ South China, Affiliated Changsha Cent Hosp, Hengyang Med Sch, Dept Neurol, Changsha, Peoples R China.;[Weng, Guomei] First Peoples Hosp Zhaoqing, Dept Neurol, Zhaoqing, Peoples R China.;[Tao, Xi] Hunan Normal Univ, Hunan Prov Peoples Hosp, Dept Neurol Rehabil, Affiliated Hosp 1, Changsha, Peoples R China.;[Deng, Mingzhu] Brain Hosp Hunan Prov, Peoples Hosp Hunan Prov 2, Dept Neurol, Changsha, Peoples R China.
通讯机构：
[Wang, Q ; Zhu, SZ] S;Southern Med Univ, Dept Neurol, Zhujiang Hosp, Guangzhou, Peoples R China.
关键词：
Parkinson’s disease;inflammation;lymphocyte-to-monocyte ratio;neutrophil-to-high-density lipoprotein ratio;neutrophil-to-lymphocyte ratio
摘要：
BACKGROUND: Inflammation plays a pivotal role in the pathogenesis of Parkinson's disease (PD). However, the correlation between peripheral inflammatory markers and the severity of PD remains unclear. METHODS: The following items in plasma were collected for assessment among patients with PD (n = 303) and healthy controls (HCs; n = 303) were assessed for the neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR) and neutrophil-to-high-density-lipoprotein ratio (NHR) in plasma, and neuropsychological assessments were performed for all patients with PD. Spearman rank or Pearson correlation was used to evaluate the correlation between the NLR, the LMR and the NHR and the severity of PD. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic performance of the NLR, LMR and NHR for PD. RESULTS: The plasma NLR and NHR were substantially higher in patients with PD than in HCs, while the plasma LMR was substantially lower. The plasma NLR was positively correlated with Hoehn and Yahr staging scale (H&Y), Unified Parkinson's Disease Rating Scale (UPDRS), UPDRS-I, UPDRS-II, and UPDRS-III scores. Conversely, it exhibited a negative relationship with Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) scores. Furthermore, the plasma NHR was positively correlated with H&Y, UPDRS, UPDRS-I, UPDRS-II and UPDRS-III scores. Moreover, negative associations were established between the plasma LMR and H&Y, UPDRS, UPDRS-I, UPDRS-II, and UPDRS-III scores. Finally, based on the ROC curve analysis, the NLR, LMR and NHR exhibited respectable PD discriminating power. CONCLUSION: Our research indicates that a higher NLR and NHR and a lower LMR may be relevant for assessing the severity of PD and appear to be promising disease-state biomarker candidates.
摘要：
BACKGROUND: Depression is a highly prevalent comorbidity arising in patients with Parkinson's disease (PD). However, depression in patients with PD is poorly treated. Hydrogen sulfide (H(2)S), a neuromodulator, has the potential to relieve depression. OBJECTIVE: To investigate whether H(2)S attenuates depression-like behaviours in a rat model of PD and examine the underlying mechanisms. METHODS: We utilised rotenone to develop a PD model with subcutaneous injections in the dorsal cervical region of Sprague-Dawley rats. The depression-like behaviours in the rotenone-induced PD model rats were assessed through forced swimming, tail suspension, open field, novelty-suppressed feeding, and elevated plus-maze tests. The expression of postsynaptic density protein-95 and synapsin-1, related to synaptic plasticity, was detected using Western blot in the hippocampus. The hippocampal ultrastructure, including the synaptic density, length of the synaptic active zone, postsynaptic density thickness, and synaptic gap width, was detected using transmission electron microscopy. RESULTS: We proved that sodium hydrosulfide (NaHS; a donor of H(2)S) significantly attenuated the depression-like behaviours and disorders of hippocampal synaptic plasticity in rotenone-induced PD rats. Furthermore, inhibition of the hippocampal Warburg effect by 2-deoxyglucose abolished NaHS-enhanced hippocampal synaptic plasticity and reversed NaHS-attenuated depression-like behaviours in the rotenone-induced PD rats. CONCLUSION: H(2)S attenuates PD-associated depression by improving the hippocampal synaptic plasticity in a hippocampal Warburg effect-dependent manner.
通讯作者：
Manbo Cai<&wdkj&>Xiaoming Xie<&wdkj&>Yutian Zou<&wdkj&>Manbo Cai Manbo Cai Manbo Cai<&wdkj&>Xiaoming Xie Xiaoming Xie Xiaoming Xie<&wdkj&>Yutian Zou Yutian Zou Yutian Zou
作者机构：
[Hongbo Zhu; Manbo Cai; Hongbo Zhu Hongbo Zhu Hongbo Zhu; Manbo Cai Manbo Cai Manbo Cai] The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China;[Jindong Xie; Xinpei Deng; Yi Xie; Peng Liu; Wei Deng; Li Ning; Yuhui Tang; Yuying Sun; Hailin Tang; Xiaoming Xie; Yutian Zou; Jindong Xie Jindong Xie Jindong Xie; Xinpei Deng Xinpei Deng Xinpei Deng; Yi Xie Yi Xie Yi Xie; Peng Liu Peng Liu Peng Liu; Wei Deng Wei Deng Wei Deng; Li Ning Li Ning Li Ning; Yuhui Tang Yuhui Tang Yuhui Tang; Yuying Sun Yuying Sun Yuying Sun; Hailin Tang Hailin Tang Hailin Tang; Xiaoming Xie Xiaoming Xie Xiaoming Xie; Yutian Zou Yutian Zou Yutian Zou] State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China
通讯机构：
[Manbo Cai; Manbo Cai Manbo Cai Manbo Cai] T;[Xiaoming Xie; Yutian Zou; Xiaoming Xie Xiaoming Xie Xiaoming Xie; Yutian Zou Yutian Zou Yutian Zou] S;The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China<&wdkj&>State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China
摘要：
Flowchart of our study. By utilizing multi‐omics pan‐cancer cohorts, our study firstly offers a pan‐cancer blueprint of the molecular and clinical characteristics of disulfidptosis regulators, as wells as disulfidptosis activity, which lay a solid foundation for the disulfidptosis‐targeting strategy in precision cancer treatment. Abstract Disruption of disulfide homeostasis during biological processes can have fatal consequences. Excess disulfides induce cell death in a novel manner, termed as “disulfidptosis.” However, the specific mechanism of disulfidptosis has not yet been elucidated. To determine the cancer types sensitive to disulfidptosis and outline the corresponding treatment strategies, we firstly investigated the crucial functions of disulfidptosis regulators pan‐cancer at multi‐omics levels. We found that different tumor types expressed dysregulated levels of disulfidptosis regulators, most of which had an impact on tumor prognosis. Moreover, we calculated the disulfidptosis activity score in tumors and validated it using multiple independent datasets. Additionally, we found that disulfidptosis activity was correlated with classic biological processes and pathways in various cancers. Disulfidptosis activity was also associated with tumor immune characteristics and could predict immunotherapy outcomes. Notably, the disulfidptosis regulator, glycogen synthase 1 (GYS1), was identified as a promising target for triple‐negative breast cancer and validated via in vitro and in vivo experiments. In conclusion, our study elucidated the complex molecular phenotypes and clinicopathological correlations of disulfidptosis regulators in tumors, laying a solid foundation for the development of disulfidptosis‐targeting strategies for cancer treatment.
摘要：
Sleep deprivation (SD) is a global public health burden, and has a detrimental role in the nervous system. Retina is an important part of the central nervous system; however, whether SD affects retinal structures and functions remains largely unknown. Herein, chronic SD mouse model indicated that loss of sleep for 4 months could result in reductions in the visual functions, but without obvious morphologic changes of the retina. Ultrastructural analysis by transmission electron microscope revealed the deterioration of mitochondria, which was accompanied with the decrease of multiple mitochondrial proteins in the retina. Mechanistically, oxidative stress was provoked by chronic SD, which could be ameliorated after rest, and thus restore retinal homeostasis. Moreover, the supplementation of two antioxidants, α-lipoic acid and N-acetyl-l-cysteine, could reduce retinal reactive oxygen species, repair damaged mitochondria, and, as a result, improve the retinal functions. Overall, this work demonstrated the essential roles of sleep in maintaining the integrity and health of the retina. More importantly, it points towards supplementation of antioxidants as an effective intervention strategy for people experiencing sleep shortages.
摘要：
ATP-binding cassette protein A1 (ABCA1) is a key protein in the transport of intracellular cholesterol to the extracellular and plays an important role in reduc-ing cholesterol accumulation in surrounding tissues. Bibliometric analysis refers to the cross-science of quan-titative analysis of a variety of documents by mathemati-cal and statistical methods. It combines an analysis of structural and temporal patterns in scholarly publica-tions with a description of topic concentration and types of uncertainty. This paper analyzes the history, hotspot, and development trend of ABCA1 through bibliometrics. It will provide readers with the research status and development trend of ABCA1 and help the hot research in this field explore new research directions. After screening, the research on ABCA1 is still in a hot phase in the past 20 years. ABCA1 is emerging in previously unrelated disciplines such as cancer. There were 551 key-words and 6888 breakout citations counted by CiteSpace. The relationship between cancer and cardiovascular dis-ease has been linked by ABCA1. This review will guide readers who are not familiar with ABCA1 research to quickly understand the development process of ABCA1 and provide researchers with a possible future research focus on ABCA1. (Curr Probl Cardiol 2024;49:102036.)
期刊：
Scandinavian Journal of Immunology,2024年99(3):e13357- ISSN：0300-9475
通讯作者：
Lei, AH;Zhang, HJ
作者机构：
[Long, WeiXiang; Lei, AH; Lei, Aihua; Dai, Zhongling; Liu, Duo; Gong, Zhande; Wang, Cui] Univ South China, Inst Pathogen Biol, Sch Basic Med Sci, Hengyang Med Sch, 28 Changsheng Western Rd, Hengyang 421001, Hunan, Peoples R China.;[Long, WeiXiang; Lei, Aihua; Dai, Zhongling; Liu, Duo; Gong, Zhande; Wang, Cui] Univ South China, Hunan Prov Key Lab Special Pathogens Prevent & Con, Hengyang, Peoples R China.;[Long, WeiXiang; Lei, Aihua; Dai, Zhongling; Liu, Duo; Gong, Zhande; Wang, Cui] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Hengyang, Peoples R China.;[Zhang, Haijun] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Cardiol, 69 Chuanshan Ave, Hengyang 421000, Hunan, Peoples R China.
通讯机构：
[Lei, AH ; Zhang, HJ ] U;Univ South China, Inst Pathogen Biol, Sch Basic Med Sci, Hengyang Med Sch, 28 Changsheng Western Rd, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Cardiol, 69 Chuanshan Ave, Hengyang 421000, Hunan, Peoples R China.
关键词：
allergic airway inflammation;hormones;ILC2s
摘要：
Group 2 innate lymphoid cells (ILC2s) are a type of innate immune cells that produce a large amount of IL-5 and IL-13 and two cytokines that are crucial for various processes such as allergic airway inflammation, tissue repair and tissue homeostasis. It is known that damaged epithelial-derived alarmins, such as IL-33, IL-25 and thymic stromal lymphopoietin (TSLP), are the predominant ILC2 activators that mediate the production of type 2 cytokines. In recent years, abundant studies have found that many factors can regulate ILC2 development and function. Hormones synthesized by the body's endocrine glands or cells play an important role in immune response. Notably, ILC2s express hormone receptors and their proliferation and function can be modulated by multiple hormones during allergic airway inflammation. Here, we summarize the effects of multiple hormones on ILC2-driven allergic airway inflammation and discuss the underlying mechanisms and potential therapeutic significance.
摘要：
BACKGROUND: Neuronal ferroptosis plays a critical role in the pathogenesis of cognitive deficits. The present study explored whether artemisinin protected type 2 diabetes mellitus (T2DM) mice from cognitive impairments by attenuating neuronal ferroptosis in the hippocampal CA1 region. METHODS: STZ-induced T2DM mice were treated with artemisinin (40 mg/kg, i.p.), or cotreated with artemisinin and Nrf2 inhibitor MEL385 or ferroptosis inducer erastin for 4 weeks. Cognitive performance was determined by the Morris water maze and Y maze tests. Hippocampal ROS, MDA, GSH, and Fe(2+) contents were detected by assay kits. Nrf2, p-Nrf2, HO-1, and GPX4 proteins in hippocampal CA1 were assessed by Western blotting. Hippocampal neuron injury and mitochondrial morphology were observed using H&E staining and a transmission electron microscope, respectively. RESULTS: Artemisinin reversed diabetic cognitive impairments, decreased the concentrations of ROS, MDA and Fe(2+), and increased the levels of p-Nr2, HO-1, GPX4 and GSH. Moreover, artemisinin alleviated neuronal loss and ferroptosis in the hippocampal CA1 region. However, these neuroprotective effects of artemisinin were abolished by Nrf2 inhibitor ML385 and ferroptosis inducer erastin. CONCLUSION: Artemisinin effectively ameliorates neuropathological changes and learning and memory decline in T2DM mice; the underlying mechanism involves the activation of Nrf2 to inhibit neuronal ferroptosis in the hippocampus.
作者机构：
[Jian Peng] School of Mathematics and Statistics, Hainan University, Haikou 570228, Hainan, People’s Republic of China;[Yan Wang] Department of Neurology, The First Affiliated Hospital, University of South China, Hengyang 421001, People’s Republic of China;School of Cyberspace Security, Hainan University, Haikou 570228, Hainan, People’s Republic of China;Hainan University, Key Laboratory of Engineering Modeling and Statistical Computation of Hainan Province, Haikou 570228, China;[Jingwen Zhang] School of Mathematics and Statistics, Hainan University, Haikou 570228, Hainan, People’s Republic of China<&wdkj&>School of Cyberspace Security, Hainan University, Haikou 570228, Hainan, People’s Republic of China<&wdkj&>Hainan University, Key Laboratory of Engineering Modeling and Statistical Computation of Hainan Province, Haikou 570228, China
通讯机构：
[Haohua Wang] S;School of Mathematics and Statistics, Hainan University, Haikou 570228, Hainan, People’s Republic of China<&wdkj&>Hainan University, Key Laboratory of Engineering Modeling and Statistical Computation of Hainan Province, Haikou 570228, China
关键词：
HBV model;Information intervention;Stochastic analysis;Stationary distribution;Optimal control
摘要：
The stochastic fluctuation of information induces the dynamic behavior and disease control strategy to change in the HBV epidemic model, but how stochastic information dissemination affects them is vague. Here, we consider an HBV epidemic model with stochastic information intervention. Using the Lyapunov function, we demonstrate that the system has a unique global positive solution, in addition, we also derive the threshold dynamics to obtain sufficient conditions that can ensure the extinction and persistence, as well as stationarity of the system. Moreover, we qualify the impact of stochasticity of the information on the optimal control strategy of the HBV, indicating that while information intervention could effectively reduce the disease peak, the fluctuation will attenuate this effect, i.e., the stable information is better than the noisy one. Finally, various stochastic and optimal control simulations are performed to verify the theoretical results and verify that optimal control can accelerate the extinction of the disease.
关键词：
autophagy;seizure-induced brain injury;SIRT3;Xyloketal B
摘要：
Brain damage in children due to seizures is irreversible and has been a major public health concern. The herbal monomer Xyloketal B (Xyl-B) can be used as a neuroprotective drug because of its antioxidant, antiapoptotic, and anti-inflammatory effects but with few adverse effects. In this article, we constructed a rat developmental convulsion model and a primary hippocampal neuronal cell convulsion model, through which we studied hippocampal neuronal morphology and neuronal apoptosis using H&E staining and TUNEL staining, respectively. Moreover, we measured TNF-α, IL-6, and IL-1β inflammatory factor levels using ELISA, MDA, and SOD kits. The expression of SIRT3 in hippocampal tissues was determined by qPCR and Western blotting. The expression of autophagy-related proteins such as LC3, p62, and Beclin-1 was evaluated by Western blotting or immunohistochemistry. The role of SIRT3 and autophagic activity with Xyl-B in convulsive seizure-induced brain injury was investigated by knocking down SIRT3 expression levels. Our results showed that Xyl-B plays a neuroprotective role in convulsive seizure-induced brain injury by increasing SIRT3 expression and activating the autophagy pathway. The regulatory role of SIRT3 in the autophagy pathway with Xyl-B treatment was explored by knocking down SIRT3 expression and inhibiting autophagy. Our results revealed that SIRT3 enhances the protective effect of Xyl-B against postconvulsive brain injury by regulating AMPK/mTOR signaling-mediated autophagy.
摘要：
Asparagine, an important amino acid in mammals, is produced in several organs and is widely used for the production of other nutrients such as glucose, proteins, lipids, and nucleotides. Asparagine has also been reported to play a vital role in the development of cancer cells. Although several types of cancer cells can synthesise asparagine alone, their synthesis levels are insufficient to meet their requirements. These cells must rely on the supply of exogenous asparagine, which is why asparagine is considered a semi-essential amino acid. Therefore, nutritional inhibition by targeting asparagine is often considered as an anti-cancer strategy and has shown success in the treatment of leukaemia. However, asparagine limitation alone does not achieve an ideal therapeutic effect because of stress responses that upregulate asparagine synthase (ASNS) to meet the requirements for asparagine in cancer cells. Various cancer cells initiate different reprogramming processes in response to the deficiency of asparagine. Therefore, it is necessary to comprehensively understand the asparagine metabolism in cancers. This review primarily discusses the physiological role of asparagine and the current progress in the field of cancer research.
期刊：
Brain and Behavior,2024年14(2):e3373- ISSN：2162-3279
通讯作者：
Chen, YJ
作者机构：
[Chen, Liang; Chen, Yongjun; Xie, Yangzhi] Univ South China, Affiliated Nanhua Hosp, Hengyang Med Sch, Dept Neurol, Hengyang 421001, Peoples R China.;[Chen, Jiacheng] Univ South China, Affiliated Nanhua Hosp, Hengyang Med Sch, Dept Intens Care Unit, Hengyang, Peoples R China.
通讯机构：
[Chen, YJ ] U;Univ South China, Affiliated Nanhua Hosp, Hengyang Med Sch, Dept Neurol, Hengyang 421001, Peoples R China.
关键词：
M1/M2 polarization;neuroinflammation;Parkinson's disease;regulatory T cell;vitamin D receptor
摘要：
We explored the therapeutic effects of vitamin receptor activation by calcitriol in a mouse model of PD. We found that calcitriol is potent to protect against neuroinflammation and neuronal degeneration by boosting Treg. Vitamin D receptor may be a therapeutic option for PD. Abstract Objective Vitamin D deficiency is a risk factor for Parkinson's disease (PD) and vitamin D supplementation robustly alleviates neurodegeneration in PD models. However, the mechanisms underlying this effect require further clarification. Current evidence suggests that harnessing regulatory T cells (Treg) may mitigate neuronal degeneration. In this study, we investigated the therapeutic effects of vitamin D receptor activation by calcitriol on PD, specifically focusing on its role in Treg. Methods Hemiparkinsonian mice model was established through the injection of 6‐OHDA into the striatum. Mice were pretreated with calcitriol before 6‐OHDA injection. The motor performance, dopaminergic neuronal survival, contents of dopamine, and dopamine metabolites were evaluated. The pro‐inflammatory cytokines levels, T‐cell infiltration, mRNA expression of indicated microglial M1/M2 phenotypic markers, and microglial marker in the midbrain were detected. Populations of Treg in the splenic tissues were assessed using a flow cytometry assay. PC61 monoclonal antibody was applied to deplete Treg in vivo. Results We show that calcitriol supplementation notably improved motor performance and reduced dopaminergic degeneration in the 6‐OHDA‐induced PD model. Mechanistically, calcitriol promoted anti‐inflammatory/neuroprotective Treg and inhibited pro‐inflammatory/neurodestructive effector T‐cell generation in this model. This process significantly inhibited T‐cell infiltration in the midbrain, restrained microglial activation, microglial M1 polarization, and decreased pro‐inflammatory cytokines release. This more favorable inflammatory microenvironment rescued dopaminergic degeneration. To further verify that the anti‐inflammatory effects of calcitriol are associated with Treg expansion, we applied an antibody‐mediated Treg depletion assay. As predicted, the anti‐inflammatory effects of calcitriol in the PD model were diminished following Treg depletion. Conclusion These findings suggest that calcitriol's anti‐inflammatory and neuroprotective effects in PD are associated with its potential to boost Treg expansion.
摘要：
Curcumin (CUR) exhibits a definite curative effect in the treatment of depression. To identify potential antidepressant targets and mechanisms of action of CUR. This study used network pharmacology to explore the signaling pathways and CUR-related targets in depression. C57BL/6J mice (male,12-14weeks old) were randomly divided into four groups (n = 8): saline-treated (control mice), lipopolysaccharide (LPS, 2mg/kg/day, intraperitoneally), LPS + CUR (50mg/kg/day, intragastrically), and LPS + CUR + LY294002 (7.5mg/kg/day, intraperitoneally). After 1week, behavioral tests were performed. Then, neuronal damage in the prefrontal cortex of mice was evaluated by hematoxylin-eosin (HE) staining. We uncovered the main active mechanism of CUR against depression using Western blotting and enzyme-linked immunosorbent assay (ELISA). Gene set enrichment analysis (GSEA) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways showed that the most significantly enriched pathway in CUR against depression was the PI3K-Akt pathway. Moreover, 52 targets were significantly correlated with the PI3K-Akt signaling pathway and CUR-related targets. In addition, among the top 50 targets ranked by degree in the protein-protein interaction (PPI) network, there were 23 targets involved in the 52 intersection targets. Administration of LPS alone extended immobility time in the open field test (OFT) and tail suspension test (TST) and decreased sucrose consumption in the sucrose preference test (SPT). Pretreatment with CUR relieved LPS-induced changes in the behavioral tests, activity of the PI3K-Akt signaling pathway, neuronal damage in the prefrontal cortex (PFC), and inflammatory response. Moreover, inhibition of the PI3K-Akt signaling pathway by LY294002 blocked the therapeutic effects of CUR. Our study indicates that CUR may be an effective antidepressant agent in an LPS-induced mouse model, partly because of its anti-inflammatory action through the PI3K-Akt signaling pathway.
作者机构：
[Jin, Liang; Zhai, Jinxia; Wang, Chao; Liu, Mingjie] Department of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China;[Chen, Yongjun] Department of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Electronic address: 2212680954@qq.com
通讯机构：
[Chen, Yongjun] D;Department of Neurology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China. Electronic address:
摘要：
OBJECTIVE: This review aims to provide a comprehensive summary of the latest research progress regarding the relationship between epilepsy and circular RNA (circRNA). METHODS: Relevant literature from the PubMed database was meticulously searched and reviewed. The selected articles focused on investigating the association between epilepsy and circRNA, including studies on expression patterns, diagnostic markers, therapeutic targets, and functional mechanisms. RESULTS: Epilepsy, characterized by recurrent seizures, is a neurological disorder. Numerous studies have demonstrated significant alterations in the expression profiles of circRNA in epileptic brain tissues, animal models, and peripheral blood samples. These differential expressions of circRNA are believed to be closely linked with the occurrence and development of epilepsy. Moreover, circRNA has shown promising potential as diagnostic markers for epilepsy, as well as prognostic indicators for predicting disease outcomes. Furthermore, circRNA has emerged as a potential therapeutic target for epilepsy treatment, offering prospects for gene therapy interventions. CONCLUSION: The dysregulation of circRNA expression in epilepsy suggests its potential involvement in the pathogenesis and progression of this disorder. Identifying specific circRNA molecules associated with epilepsy may pave the way for novel diagnostic approaches and therapeutic strategies. However, further investigations are imperative to elucidate the precise functional mechanisms of circRNA in epilepsy and validate its clinical utility.
