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| 1 | Comorbid Chronic Diseases and Acute Organ Injuries Are Strongly Correlated with Disease Severity and Mortality among COVID-19 Patients: A Systemic Review and Meta-Analysis显示文摘The recent outbreak of COVID-19 has been rapidly spreading on a global scale.To date,there is no specific vaccine against the causative virus,SARS-CoV-2,nor is there an effective medicine for treating COVID-19,thus raising concerns with respect to the effect of risk factors such as clinical course and pathophysiological parameters on disease severity and outcome in patients with COVID-19.By extracting and analyzing all available published clinical data,we identified several major clinical characteristics associated with increased disease severity and mortality among patients with COVID-19.Specifically,preexisting chronic conditions such as hypertension,cardiovascular disease,chronic kidney disease,and diabetes are strongly associated with an increased risk of developing severe COVID-19;surprisingly,however,we found no correlation between chronic liver disease and increased disease severity.In addition,we found that both acute cardiac injury and acute kidney injury are highly correlated with an increased risk of COVID-19-related mortality.Given the high risk of comorbidity and the high mortality rate associated with tissue damage,organ function should be monitored closely in patients diagnosed with COVID-19,and this approach should be included when establishing new guidelines for managing these high-risk patients.Moreover,additional clinical data are needed in order to determine whether a supportive therapy can help mitigate the development of severe,potentially fatal complications,and further studies are needed to identify the pathophysiology and the mechanism underlying this novel coronavirus-associated infectious disease.Taken together,these findings provide new insights regarding clinical strategies for improving the management and outcome of patients with COVID-19. | Xinhui Wang Xuexian Fang Zhaoxian Cai Xiaotian Wu Xiaotong Gao Junxia Min Fudi Wang | 2020 | Research2020，，1： | 13 |
| 2 | Copper homeostasis and cuproptosis in health and disease显示文摘all cell types.Because the accumulation of intracellular copper can induce oxidative stress and perturbing cellular function,copper homeostasis is tightly regulated.Recent studies identified a novel copper-dependent form of cell death called cuproptosis,which is distinct from all other known pathways underlying cell death.Cuproptosis occurs via copper binding to lipoylated enzymes in the tricarboxylic acid(TCA)cycle,which leads to subsequent protein aggregation,proteotoxic stress,and ultimately cell death.Here,we summarize our current knowledge regarding copper metabolism,copper-related disease,the characteristics of cuproptosis,and the mechanisms that regulate cuproptosis.In addition,we discuss the implications of cuproptosis in the pathogenesis of various disease conditions,including Wilson’s disease,neurodegenerative diseases,and cancer,and we discuss the therapeutic potential of targeting cuproptosis. | Liyun Chen Junxia Min Fudi Wang | 2022 | Signal Transduction and Targeted Therapy2022，7，12： | 10 |
| 3 | Twa1/Gid8 is a β-catenin nuclear retention factor in Wnt signaling and colorectal tumorigenesis显示文摘 | Yi Lu Shanshan Xie Wen Zhang Cheng Zhang Cheng Gao Qiang Sun Yuqi Cai Zhangqi Xu Min Xiao Yanjun Xu Xiao Huang Ximei Wu Wei Liu Fudi Wang Yibin Kang Tianhua Zhou | 2017 | Cell Research2017，27，12： | 9 |
| 4 | The zinc transporter Slc39a5 controls glucose sensing and insulin secretion in pancreatic β-cells via Sirt1- and Pgc-1α-mediated regulation of Glut2显示文摘Zinc levels are high in pancreatic β-cells, and zinc is involved in the synthesis, processing and secretion of insulin in these cells. However, precisely how cellular zinc homeostasis is regulated in pancreatic β-cells is poorly understood. By screening the expression of 14 Slc39a metal importer family member genes, we found that the zinc transporter Slc39a5 is significantly downregulated in pancreatic β-cells in diabetic db/db mice, obese ob/ob mice and high-fat diet-fed mice. Moreover,β-cell-specific Slc39a5 knockout mice have impaired insulin secretion. In addition, Slc39a5-deficient pancreatic islets have reduced glucose tolerance accompanied by reduced expression of Pgc-1α and its downstream target gene Glut2. The down-regulation of Glut2 in Slc39a5-deficient islets was rescued using agonists of Sirt1, Pgc-1α and Ppar-γ. At the mechanistic level, we found that Slc39a5-mediated zinc influx induces Glut2 expression via Sirt1-mediated Pgc-1α activation. These findings suggest that Slc39a5 may serve as a possible therapeutic target for diabetes-related conditions. | Xinhui Wang Hong Gao Wenhui Wu Enjun Xie Yingying Yu Xuyan He Jin Li Wanru Zheng Xudong Wang Xizhi Cao Zhuoxian Meng Ligong Chen Junxia Min Fudi Wang | 2019 | Protein & Cell2019，10，6： | 6 |
| 5 | Auranofin mitigates systemic iron overload and induces ferroptosis via distinct mechanisms显示文摘Iron homeostasis is essential for health;moreover,hepcidin-deficiency results in iron overload in both hereditary hemochromatosis and iron-loading anemia.Here,we identified iron modulators by functionally screening hepcidin agonists using a library of 640 FDA-approved drugs in human hepatic Huh7 cells.We validated the results in C57BL/6J mice and a mouse model of hemochromatosis(Hfe^(−/−)mice).Our screen revealed that the anti-rheumatoid arthritis drug auranofin(AUR)potently upregulates hepcidin expression.Interestingly,we found that canonical signaling pathways that regulate iron,including the Bmp/Smad and IL-6/Jak2/Stat3 pathways,play indispensable roles in mediating AUR’s effects.In addition,AUR induces IL-6 via the NF-κB pathway.In C57BL/6J mice,acute treatment with 5 mg/kg AUR activated hepatic IL-6/hepcidin signaling and decreased serum iron and transferrin saturation.Whereas chronically treating male Hfe^(−/−)mice with 5 mg/kg AUR activated hepatic IL-6/hepcidin signaling,decreasing systemic iron overload,but less effective in females.Further analyses revealed that estrogen reduced the ability of AUR to induce IL-6/hepcidin signaling in Huh7 cells,providing a mechanistic explanation for ineffectiveness of AUR in female Hfe^(−/−)mice.Notably,high-dose AUR(25 mg/kg)induces ferroptosis and causes lipid peroxidation through inhibition of thioredoxin reductase(TXNRD)activity.We demonstrate the ferroptosis inhibitor ferrostatin significantly protects liver toxicity induced by highdose AUR without comprising its beneficial effect on iron metabolism.In conclusion,our findings provide compelling evidence that TXNRD is a key regulator of ferroptosis,and AUR is a novel activator of hepcidin and ferroptosis via distinct mechanisms,suggesting a promising approach for treating hemochromatosis and hepcidin-deficiency related disorders. | Lei Yang Hao Wang Xiang Yang Qian Wu Peng An Xi Jin Weiwei Liu Xin Huang Yuzhu Li Shiyu Yan Shuying Shen Tingbo Liang Junxia Min Fudi Wang | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 5 |
| 6 | The structure of erastin-bound xCT-4F2hc complex reveals molecular mechanisms underlying erastin-induced ferroptosis显示文摘Dear Editor,Ferroptosis is an iron-dependent,non-apoptotic form of regulated cell death characterized by an accumulation of lipid.derived reactive oxygen species(ROS).The small-molecule compo und erastin in duces ferroptosis via in hibiti ng the cystineglutamate antiporter system x_(c).which consists of two subunits,namely the light chain xCT and the heavy chain 4F2hc(encoded by the SLC7A11 and SLC3A2 genes,respectively).^(1-4) | Renhong Yan Enjun Xie Yaning Li Jin Li Yuanyuan Zhang Ximin Chi Xueping Hu Lei xu Tingjun Hou Brent R.Stockwell Junxia Min Qiang Zhou Fudi Wang | 2022 | Cell Research2022，32，7： | 4 |
| 7 | DHODH tangoing with GPX4 on the ferroptotic stage显示文摘Ferroptosis,an iron-dependent form of regulated cell death,is prevented by activity of the glutathione-dependent phospholipid hydroperoxidase GPX4(Glutathione peroxidase 4)in the cytosol and mitochondria,and by the glutathione-independent CoQ10 oxidoreductase FSP1 at the plasma membrane.In their recent paper published in Nature,Mao et al.report that DHODH(Dihydroorotate dehydrogenase)coordinates with GPX4 to block ferroptosis in the mitochondrial inner membrane by reducing ubiquinone to form ubiquinol in cancer cells,thus providing a novel targeted strategy for treating cancer. | Fudi Wang Junxia Min | 2021 | Signal Transduction and Targeted Therapy2021，6，7： | 3 |
| 8 | Fighting age-related orthopedic diseases: focusing on ferroptosis显示文摘Ferroptosis, a unique type of cell death, is characterized by iron-dependent accumulation and lipid peroxidation. It is closely related to multiple biological processes, including iron metabolism, polyunsaturated fatty acid metabolism, and the biosynthesis of compounds with antioxidant activities, including glutathione. In the past 10 years, increasing evidence has indicated a potentially strong relationship between ferroptosis and the onset and progression of age-related orthopedic diseases, such as osteoporosis and osteoarthritis. Therefore, in-depth knowledge of the regulatory mechanisms of ferroptosis in age-related orthopedic diseases may help improve disease treatment and prevention. This review provides an overview of recent research on ferroptosis and its influences on bone and cartilage homeostasis. It begins with a brief overview of systemic iron metabolism and ferroptosis,particularly the potential mechanisms of ferroptosis. It presents a discussion on the role of ferroptosis in age-related orthopedic diseases, including promotion of bone loss and cartilage degradation and the inhibition of osteogenesis. Finally, it focuses on the future of targeting ferroptosis to treat age-related orthopedic diseases with the intention of inspiring further clinical research and the development of therapeutic strategies. | Qin Ru Yusheng Li Wenqing Xie Yilan Ding Lin Chen Guodong Xu Yuxiang Wu Fudi Wang | 2023 | Bone Research2023，11，1： | 2 |
| 9 | Acrodermatitis enteropathica mutations affect transport activity,localization and zinc-responsive trafficking of the mouse ZIP4 zinc transporter显示文摘 | Fudi Wang Byung-Eun Kim | 2004 | Human Molecular Genetics2004，5，： | 1 |
| 10 | structure,function,and regulation of a subfamily of mouse zinc transporter genes显示文摘 | Jodi DBS Joshua L Fudi Wang | 2003 | Biol Chem2003，278，50： | 1 |
| 11 | VPS34的乙酰化调控其脂激酶活性和经典/非经典自噬的启动显示文摘文章简介作为哺乳动物中唯一的Ⅲ型磷脂酰肌醇激酶(PI3K-Ⅲ),VPS34催化底物磷脂酰肌醇(PI)磷酸化生成的3-磷酸磷脂酰肌醇(PI3P)为自噬小体形成所必需。迄今的研究表明,VPS34与其调控蛋白作用形成的VPS34-p150-Beclin 1核心复合物是激活其活性的主要机制。 | Hua Su Fei Yang Qiuting Wang Qiuhong Shen Jingtao Huang Chao Peng Yi Zhang Wei Wan Catherine C.L.Wong Qiming Sun Fudi Wang Tianhua Zhou 刘伟 | 2018 | 科学新闻2018，0，4： | 1 |
| 12 | Rewiring ERBB3 and ERK signaling confers resistance to FGFR1 inhibition in gastrointestinal cancer harbored an ERBB3-E928G mutation显示文摘Dear Editor,Recently,a large number of studies found that activation of ERBB3(Erb-B2 receptor tyrosine kinase 3,also known as HER3)may be one of the major mechanisms underlying resistance to therapies that target the EGFR(epidermal growth factor receptor),HER2,and other receptor tyrosine kinases(RTKs)(Chen et al.,2011;Choi et al.,2012;Ross et al.,2018).Interestingly,mutations in ERBB3 are commonly reported in gastrointestinal(Gl)cancer,with mutations identified in approximately 12%of stomach and colorectal cancer cases(Jaiswal et al.,2013). | Xiang Yang Hongxiao Wang Enjun Xie Biyao Tang Qingdian Mu Zijun Song Junyi Chen Fudi Wang Junxia Min | 2020 | Protein & Cell2020，11，12： | 1 |
| 13 | Acrodermatitis enteropathica mutations affect transport activity,localization and zinc-responsive trafficking of the mouse Zip4 zinc transporter显示文摘 | Wang Fudi Byung-Eun Kim Jodi Dufner-Beattie | 2004 | Human Molecular Genetics2004，13，5： | 1 |
| 14 | Heat Treatment Promotes Ubiquitin-Mediated Proteolysis of SARS-CoV-2 RNA Polymerase and Decreases Viral Load显示文摘Despite extensive eforts,COVID-19 pandemic caused by the SARS-CoV-2 virus is still at large.Vaccination is an eftive approach to curb virus spread,but several variants(eg.delta,delta plus,omicron,and IHU)appear to weaken or possibly escape immune protection.Thus,novel and quickly scalable approaches to restrain SARS-CoV-2 are urgently needed.Mutiple evidences showed thermal sensitivity of SARS-CoV-2 and negative correlation between environmental temperature and COVID-19 transmission with unknown mechanism.Here.we reveal a potential mechanism by which mild heat treatment destabilizes the wild-type RNA-dependent RNA polymerase(also known a nonstructural protein 12(NSP12))of SARS-CoV-2 as well as the P323L mutant commonly found in SARS-CoV-2 variants,including omicron and IHU.Mechanistically,heat treatment promotes E3 ubiquitin ligase ZNF598-dependent NSP12 ubiquitination leading to proteasomal degradation and significantly decreases SARS-CoV-2 RNA copy number and viral titer.A mild daily heat Ireatment maintains low levels of both wild-type and P323L mutant of NSP12,sugesting clinical potential.Collctivel',this novel mechanism,heat-induced NSP12 degradation,suggests a prospective heat-based intervention against SARS-CoV-2. | Yasen Maimaitiyiming Tao Yang Qian Qian Wang Yan Feng Zhi Chen Mikael Bjorklund Fudi Wang Chonggao Hu Chih-Hung Hsu Hua Naranmandura | 2022 | Research2022，，2： | 1 |
| 15 | Spectroscopic Measurements of Impurity Spectra on the EAST Tokamak显示文摘Ultraviolet (UV) and visible impurity spectra (200~750 nm) are commonly used to study plasma and wall interactions in magnetic fusion plasmas. Two optical multi-channel analysis (OMA) systems have been installed for the UV-visible spectrum measurement on EAST. These two OMA systems are both equipped with the Czerny-Turner (C-T) type spectrometer. The upper vacuum vessel and inner divertor baffle can be viewed simultaneously through two optical lenses. The OMA1 system is mainly used for multi-impurity lines radiation measurement. A 280 nm wavelength range can be covered by a 300 mm focal length spectrometer equipped with a 300 grooves/mm grating. The Dα/Hα line shapes can be resolved by the OMA2 system. The focal length is 750 mm. The spectral resolution can be up to 0.01 nm using a 1800 grooves/mm grating. The impurity behaviour and hydrogen ratio evolution after boroniztion, lithium coating, and siliconization are compared. Lithium coating has shown beneficial effects on the reduction of edge recycling and low Z impurity (C,O) influx. The impurity expelling effect of the divertor configuration is also briefly discussed through multi-channels observation of OMA1 system. | FU Jia LI Yingying SHI Yuejiang WANG Fudi ZHANG Wei LV Bo HUANG Juan WAN Baonian ZHOU Qian | 2012 | Plasma Science and Technology2012，14，12： | 1 |
| 16 | Macrophage-Mediated Defensive Mechanisms Involving Zinc Homeostasis in Bacterial Infection显示文摘Zinc homeostasis in macrophages is essential for maintaining their antimicrobial functions,and a growing body of evidence indicates that both zinc depletion and excess zinc in myeloid cells decrease bacterial survival.In macrophages,maintaining intracellular and extracellular zinc levels via zinc transporter proteins,including Slc30a and Slc39a family members,plays an important role in the response to immunological signals and infection.Recently,studies have found that macrophages utilize a variety of zinc-modulating mechanisms,thus expanding our knowledge regarding the role that zinc plays in response to bacterial infection.Here,we review recent progress with respect to altered zinc metabolism in macrophages and the consequences with respect to fighting invading pathogens. | Pinanong Na-Phatthalung Junxia Min Fudi Wang | 2021 | Infectious Microbes & Diseases2021，3，4： | 1 |
| 17 | Mechanisms and regulation of defensins in host defense显示文摘As a family of cationic host defense peptides,defensins are mainly synthesized by Paneth cells,neutrophils,and epithelial cells,contributing to host defense.Their biological functions in innate immunity,as well as their structure and activity relationships,along with their mechanisms of action and therapeutic potential,have been of great interest in recent years.To highlight the key research into the role of defensins in human and animal health,we first describe their research history,structural features,evolution,and antimicrobial mechanisms.Next,we cover the role of defensins in immune homeostasis,chemotaxis,mucosal barrier function,gut microbiota regulation,intestinal development and regulation of cell death.Further,we discuss their clinical relevance and therapeutic potential in various diseases,including infectious disease,inflammatory bowel disease,diabetes and obesity,chronic inflammatory lung disease,periodontitis and cancer.Finally,we summarize the current knowledge regarding the nutrient-dependent regulation of defensins,including fatty acids,amino acids,microelements,plant extracts,and probiotics,while considering the clinical application of such regulation.Together,the review summarizes the various biological functions,mechanism of actions and potential clinical significance of defensins,along with the challenges in developing defensins-based therapy,thus providing crucial insights into their biology and potential clinical utility. | Jie Fu Xin Zong Mingliang Jin Junxia Min Fudi Wang Yizhen Wang | 2023 | Signal Transduction and Targeted Therapy2023，8，9： | 1 |
| 18 | Targeting ferroptosis opens new avenues for the development of novel therapeutics显示文摘Ferroptosis is an iron-dependent form of regulated cell death with distinct characteristics,including altered iron homeostasis,reduced defense against oxidative stress,and abnormal lipid peroxidation.Recent studies have provided compelling evidence supporting the notion that ferroptosis plays a key pathogenic role in many diseases such as various cancer types,neurodegenerative disease,diseases involving tissue and/or organ injury,and inflammatory and infectious diseases. | Shumin Sun Jie Shen Jianwei Jiang Fudi Wang Junxia Min | 2023 | Signal Transduction and Targeted Therapy2023，8，10： | 0 |
| 19 | YTHDF2-mediated regulations bifurcate BHPF-induced programmed cell deaths显示文摘N6-methyladenosine(m^(6)A)is a critical regulator in the fate of RNA,but whether and how m^(6)A executes its functions in different tissues remains largely obscure.Here we report downregulation of a crucial m^(6)A reader,YTHDF2,leading to tissue-specific programmed cell deaths(PCDs)upon fluorene-9-bisphenol(BHPF)exposure.Currently,Bisphenol A(BPA)substitutes are widely used in plastic manufacturing.Interrogating eight common BPA substitutes,we detected BHPF in 14%serum samples of pregnant participants.In a zebrafish model,BHPF caused tissue-specific PCDs triggering cardiac and vascular defects.Mechanistically,BHPF-mediated downregulation of YTHDF2 reduced YTHDF2-facilitated translation of m^(6)A-gch1 for cardiomyocyte ferroptosis,and decreased YTHDF2-mediated m^(6)A-sting1 decay for caudal vein plexus(CVP)apoptosis.The two distinct YTHDF2-mediated m^(6)A regulations and context-dependent co-expression patterns of gch1/ythdf2 and tnfrsf1a/ythdf2 contributed to YTHDF2-mediated tissue-specific PCDs,uncovering a new layer of PCD regulation.Since BHPF/YTHDF2-medaited PCD defects were also observed in mammals,BHPF exposure represents a potential health threat. | Jiebo Lin Guankai Zhan Jinfeng Liu Yasen Maimaitiyiming Zhiping Deng Baohua Li Kunhui Su Jiafeng Chen Siqi Sun Wanlin Zheng Xianghui Yu Feng He Xiaodong Cheng Lingfang Wang Bin Shen Ziqin Yao Xinquan Yang Jian Zhang Wentao He Hengyu Wu Hua Naranmandura Kao-Jung Chang Junxia Min Jun Ma Mikael Björklund Peng-Fei Xu Fudi Wang Chih-Hung Hsu | 2023 | National Science Review2023，10，12： | 0 |
| 20 | Zooming in and out of ferroptosis in human disease显示文摘Ferroptosis is defined as an iron-dependent regulated form of cell death driven by lipid peroxidation.In the past decade,it has been implicated in the pathogenesis of various diseases that together involve almost every organ of the body,including various cancers,neurodegenerative diseases,cardiovascular diseases,lung diseases,liver diseases,kidney diseases,endocrine metabolic diseases,iron-overload-related diseases,orthopedic diseases and autoimmune diseases.Understanding the underlying molecular mechanisms of ferroptosis and its regulatory pathways could provide additional strategies for the management of these disease conditions.Indeed,there are an expanding number of studies suggesting that ferroptosis serves as a bona-fide target for the prevention and treatment of these diseases in relevant pre-clinical models.In this review,we summarize the progress in the research into ferroptosis and its regulatory mechanisms in human disease,while providing evidence in support of ferroptosis as a target for the treatment of these diseases.We also discuss our perspectives on the future directions in the targeting of ferroptosis in human disease. | Xue Wang Ye Zhou Junxia Min Fudi Wang | 2023 | Frontiers of Medicine2023，17，2： | 0 |
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