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CRISPR-Cas9 gene editing strengthens cuproptosis/chemodynamic/ferroptosis synergistic cancer therapy

Acta Pharmaceutica Sinica B 2024年第9期14卷 4059-4072页

作者： Xiaoyu Wu Zijun Bai Hui Wang Hanqing Wang Dahai Hou Yunzhu Xu Guanqun Wo Haibo Cheng Dongdong Sun Weiwei Tao department of Surgical Oncology Affiliated Hospital of Nanjing University of Chinese MedicineNanjing 210029China School of Integrated Medicine Nanjing University of Chinese MedicineNanjing 210023China Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine in Prevention and Treatment of Tumor Nanjing University of Chinese MedicineNanjing 210023China School of pharmacology Nanjing University of Chinese MedicineNanjing 210023China School of pharmacology Ningxia Medical UniversityYinchuan 750004China

Copper-based nanomaterials demonstrate promising potential in cancer *** efficiently triggers a Fenton-like reaction and further consumes the high level of glutathione,initiating chemical dynamic therapy(CDT)and ***,a newly identified cell death modality that represents a great prospect in cancer therapy,is ***,active homeostatic systems rigorously keep copper levels within cells exceptionally low,which hinders the application of cooper nanomaterials-based ***,a novel strategy of CRISPR-Cas9 RNP nanocarrier to deliver cuprous ions and suppress the expression of copper transporter protein ATP7A for maintaining a high level of copper in cytoplasmic fluid is *** Cu2O and organosilica shell would degrade under the high level of glutathione and weak acidic environment,further releasing RNP and *** liberated Cut triggered a Fenton-like reaction for CDT and partially transformed to Cu2t,consuming intracellular GSH and initiating cuproptosis and ferroptosis ***,the release of RNP effectively reduced the expression of copper transporter ATP7A,subsequently increasing the accumulation of cooper and enhancing the efficacy of CDT,cuproptosis,and *** tumor microenvironment responsive multimodal nanoplatform opens an ingenious avenue for colorectal cancer therapy based on gene editing enhanced synergistic cuproptosis/CDT/ferroptosis.

关键词： GSH-and pH-responsive Effective copper delivery CRISPR-Cas9 ATP7A Cuproptosis Chemodynamic Ferroptosis Synergistic therapy

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A naturally derived small molecule compound suppresses tumor growth and metastasis in mice by relieving p53-dependent repression of CDK2/Rb signaling and the Snail-driven EMT

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Chinese Journal of Natural Medicines 2024年第2期22卷 112-126页

作者： REN Boxue LI Yang DI Lei CHENG Ranran LIU Lijuan LI Hongmei LI Yi TANG Zhangrui YAN Yongming LU Tao FU Rong CHENG Yongxian WU Zhaoqiu State Key Laboratory of Natural Medicines Department of PharmacologySchool of PharmacyChina Pharmaceutical UniversityNanjing 211198China Institute for Inheritance-Based Innovation of Chinese Medicine School of Pharmaceutical SciencesShenzhen University Health Science CenterShenzhen 518060China

The tumor suppressor protein p53 is central to cancer biology,with its pathway reactivation emerging as a promising therapeutic strategy in *** study introduced LZ22,a novel compound that selectively inhibits the growth,migration,and metastasis of tumor cells expressing wild-type p53,demonstrating ineffectiveness in cells devoid of p53 or those expressing mutant ***22’s mechanism of action involves a high-affinity interaction with the histidine-96 pocket of the MDM2 *** interaction disrupted the MDM2-p53 binding,consequently stabilizing p53 by shielding it from proteasomal ***22 impeded cell cycle progression and diminished cell proliferation by reinstating the p53-dependent suppression of the CDK2/Rb signaling ***,LZ22 alleviated the p53-dependent repression of Snail transcription factor expression and its consequent EMT,effectively reducing tumor cell migration and distal ***,LZ22 administration in tumor-bearing mice did not manifest notable side *** findings position LZ22 as a structurally unique reactivator of p53,offering therapeutic promise for the management of human cancers with wild-type TP53.

关键词： LZ22 Wild-type p53 p53 Reactivator Snail-driven EMT Tumor growth and metastasis

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Astrocytic calcium waves:unveiling their roles in sleep and arousal modulation

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Neural Regeneration Research 2024年第5期19卷 984-987页

作者： Erxi Wu Dan Qi Damir Nizamutdinov Jason H.Huang department of Neurosurgery and neuroscience Institute Baylor Scott&White HealthTempleTXUSA Texas A&M University School of Medicine TempleTXUSA Texas A&M University School of Pharmacy College StationTXUSA LIVESTRONG Cancer Institutes and department of Oncology Dell Medical Schoolthe University of Texas at AustinAustinTXUSA department of Neurosurgery Baylor College of MedicineTempleTXUSA

Neuron-astrocyte interactions are vital for the brain’s *** astrocyte activities is crucial for comprehending the complex neural network,particularly the population-level functions of neurons in different cortical states and associated behaviors in *** on animal sleep and wakefulness have revealed distinct cortical synchrony patterns between ***,outnumbering neurons by nearly fivefold,support and regulate neuronal and synaptic *** research on astrocyte activation during cortical state transitions has emphasized the influence of norepinephrine as a neurotransmitter and calcium waves as key components of ion channel *** summary focuses on a few recent studies investigating astrocyte-neuron interactions in mouse models during sleep,wakefulness,and arousal levels,exploring the involvement of noradrenaline signaling,ion channels,and glutamatergic signaling in different cortical *** findings highlight the significant impact of astrocytes on large-scale neuronal networks,influencing brain activity and *** astrocytic signaling pathways shows promise for treating sleep disorders and arousal *** research is needed to understand astrocytic calcium signaling in different brain regions and its implications for dysregulated brain states,requiring future human studies to comprehensively investigate neuron-astrocyte interactions and pave the way for therapeutic interventions in sleep-and arousal-related disorders.

关键词： arousal astrocyte calcium waves locus coeruleus neuron-astrocyte interaction norepinephrine sleep wakefulness

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Modulation of p75 neurotrophin receptor mitigates brain damage following ischemic stroke in mice

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Neural Regeneration Research 2024年第10期19卷 2093-2094页

作者： Golnoush Mirzahosseini Tauheed Ishrat department of Anatomy and Neurobiology College of MedicineThe University of Tennessee Health Science CenterMemphisTNUSA Pharmaceutical Sciences College of PharmacyThe University of Tennessee Health Science CenterMemphisTNUSA neuroscience Institute The University of Tennessee Health Science CenterMemphisTNUSA

Stroke is a significant leading cause of death and disability in the United States(Tsao et al.,2022).Approximately 87% of strokes fall into the ischemic category,mainly caused by arterial blockage(Jayaraj et al.,2019).Although the only FDA-approved effective medication is tissue plasminogen activator(tPA),it should be administrated within 4.5 hours of ischemic ***,tPA has been an integral part of managing acute ischemic stro ke.

关键词： damage arterial death p75

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Investigating causal links between gastroesophageal reflux disease and essential hypertension

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World Journal of Clinical Cases 2024年第14期12卷 2304-2307页

作者： Gowthami Sai Kogilathota Jagirdhar Yatinder Bains Salim Surani department of Medicine Saint Francis Health Science CenterNewarkNJ 07107United States department of Gastroenterology Saint Michaels Medical CenterNewarkNJ 07102United States department of Medicine and pharmacology Texas A&M UniversityCollege StationTX 77843United States

Gastroesophageal reflux disease(GERD)is a prevalent global health concern with a rising *** risk factors,including obesity,hiatal hernia,and smo-king,contribute to its *** research suggests associations bet-ween GERD and metabolic syndrome,cardiac diseases,and hypertension(HTN).Mechanisms linking GERD to HTN involve autonomic dysfunction,inflammatory states,and endothelial ***,GERD medications such as pro-ton-pump inhibitors may impact blood pressure ***,antihy-pertensive medications like beta-blockers and calcium channel blockers can exacerbate GERD *** bidirectional causality exists between GERD and HTN,longitudinal studies are warranted to elucidate the precise *** of GERD,including anti-reflux surgery,may positively influence HTN ***,the interplay of lifestyle factors,comorbidities,and medications necessitates further investigation to comprehensively understand this *** this editorial,we comment on the article published by Wei et al in the recent issue of the World Journal of Clinical *** evaluate their claims on the causal association between GERD and HTN.

关键词： Gastroesophageal reflux disease Hypertension Metabolic syndrome Gastro-esophageal reflux disease Hiatal hernia

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Repressing iron overload ameliorates central poststroke pain via the Hdac2-Kv1.2 axis in a rat model of hemorrhagic stroke

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Neural Regeneration Research 2024年第12期19卷 2708-2722页

作者： He Fang Mengjie Li Jingchen Yang Shunping Ma Li Zhang Hongqi Yang Qiongyan Tang Jing Cao Weimin Yang department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina department of Molecular Neuropathology Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina department of Nutrition The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina department of Neurology Henan Provincial People’s HospitalZhengzhouHenan ProvinceChina department of Human Anatomy School of Basic Medical SciencesZhengzhou UniversityZhengzhouHenan ProvinceChina neuroscience Research Institute Zhengzhou University Academy of Medical SciencesZhengzhouHenan ProvinceChina

Thalamic hemorrhage can lead to the development of central post-stroke *** in histone acetylation levels,which are regulated by histone deacetylases,affect the excitability of neurons surrounding the hemorrhagic ***,the regulato ry mechanism of histone deacetylases in central post-stroke pain remains unclea ***,we show that iron overload leads to an increase in histone deacetylase 2expression in damaged ventral posterolateral nucleus *** this increase restored histone H3 acetylation in the Kcna2 promoter region of the voltage-dependent potassium(Kv)channel subunit gene in a rat model of central post-stroke pain,thereby increasing Kcna2expression and relieving central ***,in the absence of nerve injury,increasing histone deacetylase 2 expression decreased Kcna2expression,decreased Kv current,increased the excitability of neurons in the ventral posterolateral nucleus area,and led to neuropathic pain ***,treatment with the iron chelator deferiprone effectively reduced iron overload in the ventral posterolateral nucleus after intracerebral hemorrhage,reversed histone deacetylase 2 upregulation and Kv1.2 downregulation,and alleviated mechanical hypersensitivity in central post-stroke pain *** results suggest that histone deacetylase 2 upregulation and Kv1.2 downregulation,mediated by iron overload,are important factors in central post-stroke pain pathogenesis and co uld se rve as new to rgets for central poststroke pain treatment.

关键词： central post-stroke pain hemorrhagic stroke histone deacetylase iron overload voltage-gated potassium ion channel 1.2

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Src inhibition rescues FUNDC1-mediated neuronal mitophagy in ischaemic stroke

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Stroke & Vascular Neurology 2024年第4期9卷 367-379,I0022-I0031页

作者： Tianchi Tang Li-bin Hu Chao Ding Zhihua Zhang Ning Wang Tingting Wang Hang Zhou Siqi Xia Linfeng Fan Xiong-jie Fu Feng Yan Xiangnan Zhang Gao Chen Jianru Li department of Neurosurgery Zhejiang University School of Medicine Second Affiliated HospitalHangzhouZhejiangChina 2NeurosurgeryZhejiang University School of Medicine Second Affiliated HospitalHangzhouZhejiangChina 3Zhejiang University School of MedicineHangzhouZhejiangChina 4Zhejiang University Department of PharmacologyHangzhouZhejiangChina

Background Ischaemic stroke triggers neuronal mitophagy,while the involvement of mitophagy receptors in ischaemia/reperfusion(I/R)injury-induced neuronal mitophagy remain not fully ***,we aimed to investigate the involvement of mitophagy receptor FUN14 domain-containing 1(FUNDC1)and its modulation in neuronal mitophagy induced by I/R *** Wild-type and FUNDC1 knockout mice were generated to establish models of neuronal I/R injury,including transient middle cerebral artery occlusion(tMCAO)in vivo and oxygen glucose deprivation/reperfusion in *** outcomes of mice with two genotypes were *** mitophagy was analysed both in vivo and in *** of FUNDC1 and its regulator Src were *** impact of Src on FUNDC1-mediated mitophagy was assessed through administration of Src antagonist *** To our surprise,FUNDC1 knockout mice subjected to tMCAO showed stroke outcomes comparable to those of their wild-type *** neuronal mitophagy could be activated by I/R injury,FUNDC1 deletion did not disrupt neuronal *** activation of FUNDC1,represented by dephosphorylation of Tyr18,was detected in the early stages(within 3hours)of neuronal I/R injury;however,phosphorylated Tyr18 reappeared and even surpassed baseline levels in later stages(after 6hours),accompanied by a decrease in FUNDC1-light chain 3 *** inactivation of FUNDC1 was associated with Src activation,represented by phosphorylation of Tyr416,which changed in parallel with the level of phosphorylated FUNDC1(Tyr18)during neuronal I/R ***,FUNDC1-mediated mitophagy in neurons under I/R conditions can be rescued by pharmacological inhibition of *** FUNDC1 is inactivated by Src during the later stage(after 6hours)of neuronal I/R injury,and rescue of FUNDC1-mediated mitophagy may serve as a potential therapeutic strategy for treating ischaemic stroke.

关键词： FUNDC1 involvement injury

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Context-dependent role of sirtuin 2 in inflammation

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Neural Regeneration Research 2025年第3期20卷 682-694页

作者： NoemíSola-Sevilla Maider Garmendia-Berges MCarmen Mera-Delgado Elena Puerta department of Pharmaceutical Sciences Division of PharmacologySchool of Pharmacy and NutritionUniversity of NavarraPamplonaSpain Navarra Institute for Health Research(IdiSNA) PamplonaSpain

Sirtuin 2 is a member of the sirtuin family nicotinamide adenine dinucleotide(NAD~+)-dependent deacetylases, known for its regulatory role in different processes, including inflammation. In this context, sirtuin 2 has been involved in the modulation of key inflammatory signaling pathways and transcription factors by deacetylating specific targets, such as nuclear factor κB and nucleotide-binding oligomerization domain-leucine-rich-repeat and pyrin domain-containing protein 3(NLRP3). However, whether sirtuin 2-mediated pathways induce a pro-or an anti-inflammatory response remains controversial. Sirtuin 2 has been implicated in promoting inflammation in conditions such as asthma and neurodegenerative diseases, suggesting that its inhibition in these conditions could be a potential therapeutic strategy. Conversely, arthritis and type 2 diabetes mellitus studies suggest that sirtuin 2 is essential at the peripheral level and, thus, its inhibition in these pathologies would not be recommended. Overall, the precise role of sirtuin 2 in inflammation appears to be context-dependent, and further investigation is needed to determine the specific molecular mechanisms and downstream targets through which sirtuin 2 influences inflammatory processes in various tissues and pathological conditions. The present review explores the involvement of sirtuin 2 in the inflammation associated with different pathologies to elucidate whether its pharmacological modulation could serve as an effective strategy for treating this prevalent symptom across various diseases.

关键词： interferon inflammation lipopolysaccharide neuroinflammation NLRP3 nuclear factorκB sirtuin 2

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Removal of intrahepatic bile duct stone could reduce the risk of cholangiocarcinoma

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World Journal of Clinical Cases 2024年第11期12卷 1881-1884页

作者： Gowthami Sai Kogilathota Jagirdhar Yatinder Bains Salim Surani department of Medicine Saint Francis Health Science CenterNewarkNJ 07107United States department of Gastroenteroly Saint Michaels Medical CenterNewarkNJ 07102United States department of Medicine and pharmacology Texas A&M UniversityCollege StationTX 77843United States

Hepatolithiasis(HL)poses a significant risk for cholangiocarcinoma(CCA)development,with reported incidences ranging from 5%-13%.Risk factors include older age,smoking,hepatitis B infection,and prolonged HL *** inflammation and mechanical stress on the biliary epithelium contribute to CCA *** reduces CCA risk by removing stones and atrophic liver ***,residual stones and incomplete removal increase CCA *** et al identified carbohydrate antigen 19-9,carcinoembryonic antigen,and stone laterality as CCA risk factors,reaffirming the importance of complete stone ***,challenges remain in preventing CCA recurrence ***-term studies are needed to elucidate CCA risk factors further.

关键词： Hepatolithiasis Cholangiocarcinoma Biliary stone Common bile duct stone Cholangitis

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Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

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Neural Regeneration Research 2025年第3期20卷 613-631页

作者： Yanxin Shen Guimei Zhang Chunxiao Wei Panpan Zhao Yongchun Wang Mingxi Li Li Sun department of Neurology and neuroscience Center The First Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina Cognitive Impairment Center Department of NeurologyThe First Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinica

关键词： apoptosis ferroptosis inflammation lipid peroxidation natural plant products neurodegenerative disorder neuroprotection oxidative stress small-molecule drugs

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