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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 | 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 |
| 4 | Anti-inflammatory and Immunomodulatory Effects of Marine n-3 Polyunsaturated Fatty Acids on Human Health and Diseases显示文摘The pharmaceutical effects of n-3 polyunsaturated fatty acids(n-3 PUFAs) as dietary nutrients on human health and diseases have gained much attention and are investigated for decades. Docosahexaenoic acid(DHA), eicosapentaenoic acid(EPA) and docosapentaenoic acid(DPA) are the three major n-3 PUFAs enriched in marine organisms, such as fish, shrimp, algae, and so on. It has been well known that n-3 PUFAs, especially DHA and EPA, are beneficial in reducing the risk of cardiovascular and cerebrovascular diseases. Accumulating evidence suggests that n-3 PUFAs might cure inflammatory diseases through several mechanisms, such as plasma membrane remodeling of lymphocytes, down-regulating pro-inflammatory cytokines, and alternating adhesion molecule expressions. Several molecular targets of n-3 PUFAs on immune-regulation have also been identified, such as GPR120(FFA4), protein kinase C(PKC), and PPAR-γ. However, it remains inconclusive if dietary n-3 PUFAs function the same both in vitro and in vivo based on cohort studies. This review will focus on the molecular targets and mechanisms of anti-inflammatory and immunomodulatory effects of n-3 PUFAs on human health and diseases, such as obesity, tumor, diabetes, and autoimmune diseases. | ZHANG Yiran MIN Junxia ZHANG Lijuan | 2019 | Journal of Ocean University of China2019，18，2： | 5 |
| 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 | Overexpression of astrocyte-elevated gene-1 is associated with cervicalcarcinoma progression and angiogenesis显示文摘 | Min Long Ke Dong Ping Gao Xi Wang Li Liu Shuhui Yang Fang Lin Junxia Wei Huizhong Zhang | 2013 | Oncology Reports2013，，3： | 2 |
| 9 | Synthesis and gelation behaviors of five new dimeric cholesteryl derivatives显示文摘Five new diacid amides of di-cholesteryl L-glycinates were designed and prepared.The compounds with linkers containing 0,1, 2,3,or 4 methylene units are denoted as 1,2,3,4,and 5,respectively.Their gelation behaviors in 25 solvents were tested as novel low-molecular-mass organic gelators(LMOGs).It was shown that the length of the linker connecting the two-cholesteryl residues in a gelator plays a crucial role in the gelation behavior of the compound.1 gels 11 of the 25 solvents tested at a concentration lower than 1.0%,while 2 gels 17 of the solvents tested.4 and 5,however,gel only 2 and 4 of them,respectively. SEM observation reveals that the lengths of the linkers and the identity of the solvents are the main factors affecting the structures of the aggregates in the gels.Experimentally,a clear linker effect on the microstructures of the gels was observed.As example,the aggregates of 1,2 and 3 in benzene or 1-heptanol adopt structures of thin fibers,rods or lamellas,respectively. Furthermore,it was found that the gelation and aggregation behaviors of 2,3,4,and 5 in DMSO showed an even-odd effect. | LIU KaiQiang PENG JunXia XUE Min YAN Ni LIU Jing FANG Yu | 2011 | Science China Chemistry2011，54，3： | 2 |
| 10 | Gene therapy with RNAi targeting UHRF1 driven by tumor-specific promoter inhibits tumor growth and enhances the sensitivity of chemotherapeutic drug in breast cancer in vitro and in vivo显示文摘 | Lin Fang Li Shanqu Gao Ping He Ting Wang Xi Dong Ke Long Min Wei Junxia Zhang Huizhong | 2012 | Cancer Chemotherapy and Pharmacology2012，，： | 1 |
| 11 | 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 |
| 12 | 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 |
| 13 | 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 |
| 14 | 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 |
| 15 | 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 |
| 16 | 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 |
| 17 | Targeting the LSD1-G9a-ER Stress Pathway as a Novel Therapeutic Strategy for Esophageal Squamous Cell Carcinoma显示文摘Despite recent advances in the management and treatment of esophageal squamous cell carcinoma(ESCC),the prognosis remains extremely poor,and current nonsurgical treatment options are limited.To identify new therapeutic targets,we screened a curated library of epigenetic compounds using a panel of cancer cell lines and found that coinhibiting the histone demethylase LSD1 and the histone methyltransferase G9a potently suppresses cell growth;similar results were obtained by knocking down both LSD1 and G9a expression.Importantly,we also found that inhibiting LSD1 and G9a significantly decreased tumor growth in a xenograft mouse model with ESCC cell lines.To examine the clinical relevance of these findings,we performed immunohistochemical analyses of microarray profiling data obtained from human esophageal squamous cancer tissues and found that both LSD1 and G9a are upregulated in cancer tissues compared to healthy tissues,and this increased expression was significantly correlated with poor prognosis.Mechanistically,we discovered that inhibiting LSD1 and G9a induces cell death via S-phase arrest and apoptosis,and cotargeting ER stress pathways increased this effect both in vitro and in vivo.Taken together,these findings provide compelling evidence that targeting LSD1,G9a,and ER stress-related pathways may serve as a viable therapeutic strategy for ESCC. | Hongxiao Wang Zijun Song Enjun Xie Junyi Chen Biyao Tang Fudi Wang Junxia Min | 2022 | Research2022，，3： | 0 |
| 18 | First Beam Commissioning of SSC-Linac as an Injector of SSC显示文摘The construction of the SSC-Linac has made significant progress in 2019.The first beam commissioning of SSC-Linac as an injector of the Separated Sector Cyclotron(SSC)was performed succssfully with ^(40)Ar^(7+) beam and the particle energy of 5.98 MeV/u was obtained at the exit of SSC on December 17,2019. | Du Heng Yin Xuejun Yang Weiqing Li Zhongshan Kong Qiyu Li Xiaoni Yang Shengli Qian Cheng WangHaoning Cong Yan Jin Peng Zhang Ruifeng Han Xiaodong Fu Xin Wang Kai Jing Long Zhang Yong Li Lili Xie Wenjun Xu Xiaowei Wang Shaoming Chen Wenjun Liu Xiaojun Yue Min An Jingrui Zhang Xiang Yan Huaihai Feng Anhui Zhang Shuai Zhang Yongbo Sun Peng Zhu Tieming Sha Xiaoping Xu Jianye Sun Xiaolong Su Xuemin Li Anping Yan Tailai Meng Jun Zhang Wei Wu Junxia Yao Qinggao Yang Yaqing Xu Zhe Sun Liangting Gao Daqing Yuan Youjin Yang Jiancheng Xia Jiawen | 2019 | IMP & HIRFL Annual Report2019，，1： | 0 |
| 19 | A Systemic Review and Meta-analysis of the Effect of SARS-CoV-2 Infection on Sperm Parameters显示文摘Objective.Several studies examined the putativefets of SARS-Cov-2infectionon spem parametersHoweve,the resuls remain controversial.In this study,we conducted the most up-to-date systematic review and meta-analysis to investigate the effect of SARS-CoV-2 infection on sperm quality in COVID-19-positive and COVID-19-negative male participants.Method.Seven databases were searched forliterature released through June 10,2022,containing estimates for the outcomes of interest Using a random-fects model(REM)or a fixed-ffects model(FEM),we analyzed the pooled results.The quality of all included studies was asssed by the Newcastle-Ottawa scale In addition,we performed aquanttative and subgroup analysis of semen data across all included studies.Results.Fourteen studies were extracted from 10 publications,involving a total of 1174 participates for meta-analysis.Sperm parameters of 521 COVID-19 male patients and 653 controls were analyzed.In 8 case-control studies,the pooled mean dfference(MD)of total sperm motility was-5.37%(95%confidence interval(CI):-8.47 to-2.28:<0.05),suggesting that total motility was significantly impaired inmale COVID-19 cases.Subgroup analysis showed a significant decreasein semen volume,sperm concentration,and total motility in 238 patients with arecovery timeof less than 90 days.Moreover,in the other 6 included pre-to post-COVID-19 studies,the pooled MDs of sperm concentration,total sperm count,total motility,progressivemotility,and normal morphology were6.54×10^(6)/ml(95%CI:-10.27 to-2.81;p<0.05),38.89×10^(6)(95%CI:-59.20 to-18.58;p<0.05),-7.21%(95%CI:-14.36 to-0.07;p<0.05),-5.12%(95%CI:-8.71 to-1.53;p<0.05),and-1.52%(95%CI:-2.88 to-0.16;p<0.05),respectively,which indicate SARS-CoV-2 infection significantly affected these five sperm parameters.Conclusion.Our results revealed that SARS-CoV-2 infection was significantly correlated with decreased sperm quality.Of six sperm parameters,total motility and sperm concentration were the most significantly decreased parameters.These results suggest a possible negative influence of SARS-CoV-2 infection on testicular function and male fertility.Given the potential detrimental effect of SARS-CoV-2 on semen quality,male reproductive health should be monitored closely in patients with COVID-19.This trial is registered with CRD42021275823. | Xi Chen Jinli Ding Miao Liu Kai Xing Peng Ye Junxia Min Yan Zhang Tailang Yin | 2022 | Research2022，，2： | 0 |
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