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Epigenetic regulation of the inflammatory response in stroke

Neural Regeneration Research 2025年第11期20卷 3045-3062页

作者： Jingyi Liang Fei Yang Zixiao Li Qian Li School of Basic Medical Sciences Capital Medical UniversityBeijingChina Department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina laboratory for Clinical medicine Beijing Key Laboratory of Neural Regeneration and RepairCapital Medical UniversityBeijingChina Department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical Research Center for Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare Quality Management in Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Chinese Institute for Brain Research BeijingChina Research Unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina beijing Engineering Research Center of Digital Healthcare for Neurological Diseases BeijingChina Department of Biochemistry and molecular Biology School of Basic Medical SciencesCapital Medical UniversityBeijingChina beijing key laboratory of Cancer Invasion and Metastasis Research Capital Medical UniversityBeijingChina

Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either *** mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood–brain barrier disruption,neuronal cell death,and ultimately behavioral *** the inflammatory response has been shown to mitigate this cascade of events in experimental stroke ***,in clinical trials of anti-inflammatory agents,longterm immunosuppression has not demonstrated significant clinical benefits for *** may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in *** acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic *** agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of ***,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke *** this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome *** also discuss promising molecular targets for stroke *** evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

关键词： DNA methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding RNA RNA methylation subarachnoid hemorrhage treatment

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Endothelial mechanosensors: the gatekeepers of vascular homeostasis and adaptation under mechanical stress

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Science China(Life Sciences) 2014年第8期57卷 755-762页

作者： DENG QiuPing HUO YingQing LUO JinCai laboratory of Vascular Biology Institute of Molecular MedicineBeijing Key Laboratory of Cardiometabolic Molecular MedicinePeking University

Endothelial cells(ECs)not only serve as a barrier between blood and extravascular space to modulate the exchange of fluid,macromolecules and cells,but also play a critical role in regulation of vascular homeostasis and adaptation under mechanical stimulus via intrinsic ***,with the dissection of microdomains responsible for cellular responsiveness to mechanical stimulus,a lot of mechanosensing molecules(mechanosensors)and pathways have been identified in *** addition,there is growing evidence that endothelial mechanosensors not only serve as key vascular gatekeepers,but also contribute to the pathogenesis of various vascular *** review focuses on recent findings in endothelial mechanosensors in subcellular microdomains and their roles in regulation of physiological and pathological functions under mechanical stress.

关键词： endothelial cells mechanotransduction mechanosensors vascular adaptation vascular pathogenesis

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A unified deep-learning network to accurately segment insulin granules of different animal models imaged under different electron microscopy methodologies

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Protein & Cell 2019年第4期10卷 306-311页

作者： Xiaoya Zhang Xiaohong Peng Chengsheng Han Wenzhen Zhu Lisi Wei Yulin Zhang Yi Wang Xiuqin Zhang Hao Tang Jianshe Zhang Xiaojun Xu Fengping Feng Yanhong Xue Erlin Yao Guangming Tan Tao Xu Liangyi Chen State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing ChinaState Key Laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China Drug Discovery Center Key Laboratory of Chemical Genomics Peking University Shenzhen Graduate School Shenzhen China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China State key laboratory of Membrane Biology Beijing Key Laboratory of Cardiometabolic Molecular Medicine Institute of Molecular Medicine Peking University Beijing China University of Chinese Academy of Sciences Beijing China Marine Science College of Zhejiang Ocean University National Engineering Research Center of Marine Facilities Aquaculture Zhoushan China National laboratory of Biomacromolecules CAS Center for Excellence in Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing China National laboratory of Biomacromo

Insulin is important for body metabolism regulation and glucose homeostasis,and its dysregulation often leads to metabolic syndrome(MS)and *** is normally stored in large dense-core vesicles(LDCVs)in pancreatic beta cells,and significant reductions in the number,size,gray level and density of insulin granules confer diabetes both in mice(Xue et al.,2012)and humans(Masini et al.,2012).

关键词： deep-learning network animal

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Regulation of superoxide flashes by transient and steady mitochondrial calcium elevations

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Science China(Life Sciences) 2014年第5期57卷 495-501页

作者： JIAN ChongShu HOU TingTing YIN RongKang CHENG HePing WANG XianHua State key laboratory of Biomembrane and Membrane Biotechnology Beijing Key Laboratory of Cardiometabolic Molecular MedicineInstitute of Molecular MedicinePeking-Tsinghua Center for Life SciencesPeking University

The mitochondria play essential roles in both intracellular calcium and reactive oxygen species *** a newly discovered universal and fundamental mitochondrial phenomenon,superoxide flashes reflect transient bursts of superoxide production in the matrix of single *** and how the superoxide flash activity is regulated by mitochondrial calcium remain largely *** we demonstrate that elevating mitochondrial calcium either by the calcium ionophore ionomycin or by increasing the bathing calcium in permeabilized HeLa cells increases superoxide flash incidence,and inhibition of the mitochondrial calcium uniporter activity abolishes the flash ***,the superoxide flash incidence is correlated to the steady-state mitochondrial calcium elevation with 1.7-fold increase per 1.0?F/F0 of Rhod-2 *** contrast,large mitochondrial calcium transients(e.g.,peak△F/F0~2.8,duration^2 min)in the absence of steady-state elevations failed to alter the flash *** results indicate that physiological levels of sustained,but not transient,mitochondrial calcium elevation acts as a potent regulator of superoxide flashes,but its mechanism of action likely involves a multi-step,slow-onset process.

关键词： superoxide flash calcium signaling reactive oxygen species (ROS) mitochondrion

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Unraveling post-growth mechanisms of monolayer CsPbBr3 nanocubes:Laser-enhanced transformations and cathodoluminescence-electron microscopy correlations

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Journal of Energy Chemistry 2025年第01期 146-156页

作者： Mingxing Li Xiaoge Wang Xiaofan Cao Zhiqun He Chunjun Liang Mingxing Chen Jing Ju Fangtian You key laboratory of Luminescence and Optical Information Ministry of Education Institute of Optoelectronic Technology Beijing Jiaotong University beijing National laboratory for molecular Sciences (BNLMS) College of Chemistry and Molecular Engineering Peking University

Lead-halide perovskite nanoparticles（LHP NPs） are highly promising materials for next-generation displays and solid-state lighting due to their exceptional optical properties. However, their inherent instability presents a significant challenge. Recent advances have demonstrated that optoelectronic devices based on monolayer nanoparticle films exhibit both high luminescence efficiency and long-term *** research demonstrates that mobility limitations and anisotropic alignments in CsPbBr3nanocube monolayer films are key to their stabilization, hindering spontaneous growth through face-to-face fusion and resulting in the formation of connecting necks in a diagonal direction. Introducing laser irradiation confirmed this by significantly accelerating nanocubes growth, increasing mobility, and enhancing local structural ordering, leading to larger and more regularly shaped nanosheets. Fourier transform infrared spectroscopy and energy dispersive spectroscopy line-scan analyses indicated that laser irradiation did not disrupt the ligand structure. Transmission electron microscopy and correlative cathodoluminescence electron microscopy revealed the effects of post-growth and heterogeneous structures, including enhanced luminescence and inhomogeneous intensity in the nanosheets. These findings deepen the understanding of the post-growth mechanism of monolayer nanoparticles and the structure-emission correlation and highlight the unique role of laser irradiation in directing the formation of well-defined and regular nanostructures.

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The complex roles of m^(6)A modifications in neural stem cell proliferation, differentiation, and self-renewal and implications for memory and neurodegenerative diseases

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Neural Regeneration Research 2025年第6期20卷 1582-1598页

作者： Yanxi Li Jing Xue Yuejia Ma Ke Ye Xue Zhao Fangliang Ge Feifei Zheng Lulu Liu Xu Gao Dayong Wang Qing Xia Department of Biochemistry and molecular Biology College of Basic Medical SciencesHarbin Medical UniversityHarbinHeilongjiang ProvinceChina College of Basic Medical Sciences Harbin Medical UniversityHarbinHeilongjiang ProvinceChina Basic Medical Institute Heilongjiang Academy of Medical SciencesHarbinHeilongjiang ProvinceChina key laboratory of Heilongjiang Province for Genetically Modified Animals Harbin Medical UniversityHarbinHeilongjiang ProvinceChina Translational medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbinHeilongjiang ProvinceChina Dongzhimen Hospital Beijing University of Chinese MedicineBeijingChina

N6-methyladenosine(m^(6)A), the most prevalent and conserved RNA modification in eukaryotic cells, profoundly influences virtually all aspects of mRNA metabolism. mRNA plays crucial roles in neural stem cell genesis and neural regeneration, where it is highly concentrated and actively involved in these processes. Changes in m^(6)A modification levels and the expression levels of related enzymatic proteins can lead to neurological dysfunction and contribute to the development of neurological diseases. Furthermore, the proliferation and differentiation of neural stem cells, as well as nerve regeneration, are intimately linked to memory function and neurodegenerative diseases. This paper presents a comprehensive review of the roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, as well as its implications in memory and neurodegenerative diseases. m^(6)A has demonstrated divergent effects on the proliferation and differentiation of neural stem cells. These observed contradictions may arise from the time-specific nature of m^(6)A and its differential impact on neural stem cells across various stages of development. Similarly, the diverse effects of m^(6)A on distinct types of memory could be attributed to the involvement of specific brain regions in memory formation and recall. Inconsistencies in m^(6)A levels across different models of neurodegenerative disease, particularly Alzheimer's disease and Parkinson's disease, suggest that these disparities are linked to variations in the affected brain regions. Notably, the opposing changes in m^(6)A levels observed in Parkinson's disease models exposed to manganese compared to normal Parkinson's disease models further underscore the complexity of m^(6)A's role in neurodegenerative processes. The roles of m^(6)A in neural stem cell proliferation, differentiation, and self-renewal, and its implications in memory and neurodegenerative diseases, appear contradictory. These inconsistencies may be a

关键词： Alzheimer's disease cell self-renewal central nervous system memory microglia nerve regeneration neurodegenerative diseases neurogenesis RNA methylation

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molecular regulation of myocardial proliferation and regeneration

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Cell Regeneration 2021年第1期10卷 139-155页

作者： Lixia Zheng Jianyong Du Zihao Wang Qinchao Zhou Xiaojun Zhu Jing-Wei Xiong beijing key laboratory of cardiometabolic molecular medicine Institute of Molecular Medicine and State Key Laboratory of Natural and Biomimetic DrugsPeking UniversityBeijing 100871China

Heart regeneration is a fascinating and complex biological process. Decades of intensive studies have revealed asophisticated molecular network regulating cardiac regeneration in the zebrafish and neonatal mouse heart. Here,we review both the classical and recent literature on the molecular and cellular mechanisms underlying heartregeneration, with a particular focus on how injury triggers the cell-cycle re-entry of quiescent cardiomyocytes toreplenish their massive loss after myocardial infarction or ventricular resection. We highlight several importantsignaling pathways for cardiomyocyte proliferation and propose a working model of how these injury-inducedsignals promote cardiomyocyte proliferation. Thus, this concise review provides up-to-date research progresses onheart regeneration for investigators in the field of regeneration biology.

关键词： Cardiac regeneration Cardiomyocyte proliferation Signaling pathways Zebrafish Mouse

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Critical role of zebrafish dnajb5 in myocardial proliferation and regeneration

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Journal of Genetics and Genomics 2020年第8期47卷 493-496页

作者： Meijun Pang Connie Xiong Chenglu Xiao Jianyong Du Lixia Zheng Linlu Bai Xiaojun Zhu Jing-Wei Xiong beijing key laboratory of cardiometabolic molecular medicine Institute of Molecular Medicine and State Key Laboratory of Natural and Biomimetic DrugsPeking UniversityBeijing100871China Academy for Advanced Interdisciplinary Studies Peking UniversityBeijing100871China

Myocardial infarction is a devastating disease *** present,nearly 40 million patients suffer from heart *** to a lack of adequate blood supply,25%of cardiomyocytes are subjected to apoptosis and necrosis within a few hours after *** remains challenging to find effective therapeutic methods for heart *** the other hand,zebrafish and neonatal mouse hearts have a strong ability to regenerate(Poss et al.,2002;Raya et al.,2003;Porrello et al.,2011),and their regeneration derives from existing cardiomyocytes(Jopling et al.,2010;Kikuchi et al..

关键词： al. infarction neonatal

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Evolutionary insights into heart regeneration

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Cell Regeneration 2020年第1期9卷 270-271页

作者： Jing-Wei Xiong beijing key laboratory of cardiometabolic molecular medicine Institute of Molecular Medicineand State Key Laboratory of Natural and Biomimetic DrugsPeking UniversityBeijing 100871China

Some lower vertebrates such as zebrafish and axolotl have incredible cardiac regenerative potential while mammals have very limited *** studies among species have revealed that cardiomyocyte polyploidy,endothermy,and injury-induced activation of certain transcriptional factors including AP1 complexes are critical for cardiomyocyte proliferation and heart regeneration during animal *** insights into these evolutionarily conserved mechanisms will likely lead to achieving heart regeneration in non-regenerative mammals including humans.

关键词： evolution. mammals regeneration

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Ligand binding and conformational changes of SUR1 subunit in pancreatic ATP-sensitive potassium channels

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Protein & Cell 2018年第6期9卷 553-567页

作者： Jing-Xiang Wu Dian Ding Mengmeng Wang Yunlu Kang Xin Zeng Lei Chen State key laboratory of Membrane Biology Institute of Molecular Medicine Peking University Beijing Key Laboratory of Cardiometabolic Molecular Medicine Beijing 100871 China Peking-Tsinghua Center for Life Sciences Peking University Beijing 100871 China Academy for Advanced Interdisciplinary Studies Peking University Beijing 100871 China

ATe-sensitive potassium channels （KATP） are energy sensors on the plasma membrane. By sensing the intracellular ADP/ATP ratio of β-cells, pancreatic KATe channels control insulin release and regulate metabo- lism at the whole body level. They are implicated in many metabolic disorders and diseases and are there- fore important drug targets. Here, we present three structures of pancreatic KATe channels solved by cryo- electron microscopy （cryo-EM）, at resolutions ranging from 4.1 to 4.5 A. These structures depict the binding site of the antidiabetic drug glibenclamide, indicate how Kir6.2 （inward-rectifying potassium channel 6.2） N-ter- minus participates in the coupling between the periph- eral SUR1 （sulfonylurea receptor 1） subunit and the central Kir6.2 channel, reveal the binding mode of acti- vating nucleotides, and suggest the mechanism of how Mg-ADP binding on nucleotide binding domains （NBDs） drives a conformational change of the SUR1 subunit.

关键词： KATP SUR ABC transporter glibenclamide sulfonylurea diabetes

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