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Ischemia-reperfusion injury:molecular mechanisms and therapeutic targets

Signal Transduction and Targeted Therapy 2024年第2期9卷 558-596页

作者： Meng Zhang Qian Liu Hui Meng Hongxia Duan Xin Liu Jian Wu Fei Gao Shijun Wang Rubin Tan Jinxiang Yuan The Collaborative Innovation Center Jining Medical UniversityJiningShandong 272067China Clinical medical College Jining Medical UniversityJiningShandong 272067China Second Clinical medical College Jining Medical UniversityJiningShandong 272067China Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital and Institutes of Biomedical SciencesFudan UniversityShanghaiChina Institute of Zoology Chinese Academy of SciencesBeijingChina Department of Physiology Basic medical schoolXuzhou Medical UniversityXuzhou 221004China

Ischemia-reperfusion(I/R)injury paradoxically occurs during reperfusion following ischemia,exacerbating the initial tissue damage.The limited understanding of the intricate mechanisms underlying I/R injury hinders the development of effective therapeutic interventions.The Wnt signaling pathway exhibits extensive crosstalk with various other pathways,forming a network system of signaling pathways involved in I/R injury.This review article elucidates the underlying mechanisms involved in Wnt signaling,as well as the complex interplay between Wnt and other pathways,including Notch,phosphatidylinositol 3-kinase/protein kinase B,transforming growth factor-β,nuclear factor kappa,bone morphogenetic protein,N-methyl-D-aspartic acid receptor-Ca2+-Activin A,Hippo-Yes-associated protein,toll-like receptor 4/toll-interleukine-1 receptor domain-containing adapter-inducing interferon-β,and hepatocyte growth factor/mesenchymal-epithelial transition factor.In particular,we delve into their respective contributions to key pathological processes,including apoptosis,the inflammatory response,oxidative stress,extracellular matrix remodeling,angiogenesis,cell hypertrophy,fibrosis,ferroptosis,neurogenesis,and blood-brain barrier damage during I/R injury.Our comprehensive analysis of the mechanisms involved in Wnt signaling during I/R reveals that activation of the canonical Wnt pathway promotes organ recovery,while activation of the non-canonical Wnt pathways exacerbates injury.Moreover,we explore novel therapeutic approaches based on these mechanistic findings,incorporating evidence from animal experiments,current standards,and clinical trials.The objective of this review is to provide deeper insights into the roles of Wnt and its crosstalk signaling pathways in I/R-mediated processes and organ dysfunction,to facilitate the development of innovative therapeutic agents for I/R injury.

关键词： therapeutic reperfusion damage

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Cancer-educated neutrophils promote lung cancer progression via PARP-1-ALOX5-mediated MMP-9 expression

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Cancer Biology & Medicine 2024年第2期21卷 175-192页

作者： Lulu Han Yuxin Chen Nan Huang Xiaowan Zhou Yanfang Lv Huizhong Li Dafei Chai Junnian Zheng Gang Wang Cancer Institute Xuzhou Medical University209 Tongshan RoadXuzhou 221004China Center of Clinical Oncology The Affiliated Hospital of Xuzhou Medical University99 West Huaihai RoadXuzhou 221002China Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy Xuzhou Medical University209 Tongshan RoadXuzhou 221004China Department of Oncology Suzhou Xiangcheng People’s HospitalSuzhou 215131China

Objective:Neutrophils are one of the most predominant infiltrating leukocytes in lung cancer tissues and are associated with lung cancer progression.How neutrophils promote lung cancer progression,however,has not been established.Methods:Kaplan–Meier plotter online analysis and tissue immunohistochemistry were used to determine the relationship between neutrophils and overall survival in lung cancer patients.The effect of neutrophils on lung cancer was determined using the Transwell migration assay,a proliferation assay,and a murine tumor model.Gene knockdown was used to determine poly ADPribose polymerase(PARP)-1 function in lung cancer-educated neutrophils.Western blot analysis and gelatin zymography were used to demonstrate the correlation between PARP-1 and matrix metallopeptidase 9(MMP-9).Immunoprecipitation coupled to mass spectrometry(IP/MS)was used to identify the proteins interacting with PARP-1.Co-immunoprecipitation(Co-IP)was used to confirm that PARP-1 interacts with arachidonate 5-lipooxygenase(ALOX5).Neutrophil PARP-1 blockage by AG14361 rescued neutrophil-promoted lung cancer progression.Results:An increased number of infiltrating neutrophils was negatively associated with overall survival in lung cancer patients(P<0.001).Neutrophil activation promoted lung cancer cell invasion,migration,and proliferation in vitro,and murine lung cancer growth in vivo.Mechanistically,PARP-1 was shown to be involved in lung cancer cell-induced neutrophil activation to increase MMP-9 expression through interacting and stabilizing ALOX5 by post-translational protein modification(PARylation).Blocking PARP-1 by gene knockdown or AG14361 significantly decreased ALOX5 expression and MMP-9 production,and eliminated neutrophil-mediated lung cancer cell invasion and in vivo tumor growth.Conclusion:We identified a novel mechanism by which PARP-1 mediates lung cancer cell-induced neutrophil activation and PARylates ALOX5 to regulate MMP-9 expression,which exacerbates lung cancer progression.

关键词： Lung cancer neutrophils PARP-1 ALOX5 MMP-9

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Recent advances in ultrasound-controlled fluorescence technology for deep tissue optical imaging

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Journal of Pharmaceutical Analysis 2022年第4期12卷 530-540页

作者： Rui-Lin Liu Ru-Qian Cai School of Pharmacy Xuzhou Medical UniversityXuzhou221004China Department of Pharmaceutical Analysis School of PharmacyXi'an Jiaotong UniversityXi'an710061China

Fluorescence imaging is a noninvasive and dynamic real-time imaging technique;however,it exhibits poor spatial resolution in centimeter-deep tissues because biological tissues are highly scattering media for optical radiation.The recently developed ultrasound-controlled fluorescence(UCF)imaging is a novel imaging technique that can overcome this bottleneck.Previous studies suggest that the effective contrast agent and sensitive imaging system are the two pivotal factors for generating high-resolution UCF images ex vivo and/or in vivo.Here,this review highlights the recent advances(2015e2020)in the design and synthesis of contrast agents and the improvement of imaging systems to realize high-resolution UCF imaging of deep tissues.The imaging performances of various UCF systems,including the signal-to-noise ratio,imaging resolution,and imaging depth,are specifically discussed.In addition,the challenges and prospects are highlighted.With continuously increasing research interest in this field and emerging multidisciplinary applications,UCF imaging with higher spatial resolution and larger imaging depth may be developed shortly,which is expected to have a far-reaching impact on disease surveillance and/or therapy.

关键词： Ultrasound-controlled fluorescence imaging Temperature-sensitive NIR probes High-resolution Deep tissue Molecular diagnosis

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Bimetallic Fe-Co Nanoalloy Confined in Porous Carbon Skeleton with Enhanced Peroxidase Mimetic Activity for Multiple Biomarkers Monitoring

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Journal of Analysis and Testing 2023年第1期7卷 53-68页

作者： Jingjing Luo Ruilin Liu Shuchang Zhao Yuan Gao School of Pharmacy Xuzhou Medical UniversityXuzhou 221004China

Carbon-based nanozymes with multifunctional applications have attracted enormous attention,however,there is still a lack of an effective strategy for inexpensive preparation of high-active carbon-based nanozyme.We herein report a waste paperderived CoFe_(2)O_(4)/porous carbon nanozyme for the colorimetric detection of glucose and glutathione(GSH)in biofluids.The hybrid CoFe_(2)O_(4)/porous carbon material was successfully prepared via a combined impregnation,hydrolysis and carbonization method.Newly constructed CoFe_(2)O_(4)/porous carbon material with enhanced peroxidase-like activity could oxidize colorless tetramethylbenzidine(TMB)to blue oxidized TMB with adding H_(2)O_(2).A sensitive colorimetric analysis platform for monitoring the levels of glucose and GSH in biofluids was respectively developed.The proposed analytical method possessed predominant features such as low limit of detections(LODs)(0.16μmol/L for glucose and 120 nmol/L for GSH),broad linear ranges(1-200μmol/L for glucose and 1-50μmol/L for GSH),and excellent practical potential.This multipurpose platform not only provides a promising strategy for transforming waste paper into valuable carbon-based nanozyme,but also paves the way for excavating the potential biomedical and environmental applications from waste paper.

关键词： Carbon nanozyme Fe-Co nanoalloy Glucose Glutathione Colorimetric assay

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Recent advances in catalytic enantioselective direct C–H bond functionalization of electrondeficient N-containing heteroarenes

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Organic Chemistry Frontiers 2022年第1期9卷 265-280页

作者： Xiao-Lan Liu Luo-Bin Jiang Mu-Peng Luo Zhi Ren Shou-Guo Wang Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences1068 Xueyuan AvenueShenzhenChina College of Pharmacy Shenzhen Technology University3002 Lantian RoadShenzhenChina School of medical Imaging Xuzhou Medical UniversityXuzhouChina

Catalytic enantioselective direct C–H bond functionalization of electron-deficient N-containing heteroarenes represents one of the most straightforward and powerful protocols to construct diverse enantioenriched highly functionalized N-heteroarene products.Efficient catalytic systems and a variety of strategies for highly chemo-and stereoselective C–H functionalization of electron-deficient N-containing heteroarenes have been developed over the past few decades.This review summarized the rapid progress in the catalytic asymmetric C–H functionalization of N-containing heteroarenes and discussed the challenges and potential of the field in the current stage.

关键词： deficient catalytic enantioselective

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Ferroptosis-based nano delivery systems targeted therapy for colorectal cancer:Insights and future perspectives

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Asian Journal of Pharmaceutical Sciences 2022年第5期17卷 613-629页

作者： Chu Qiao Haiying Wang Qiutong Guan Minjie Wei Zhenhua Li School of Pharmacy China Medical UniversityShenyang 110122China

There are limited options for patients who develop liver metastasis from colorectal cancer(CRC),the leading cause of cancer-related mortality worldwide.Emerging evidence has provided insights into iron deficiency and excess in CRC.Ferroptosis is an iron-dependent form of programmed cell death characterized by aberrant iron and lipid metabolism,which play crucial roles in tumorigenesis,tumor progression,and treatment options.A better understanding of the underlying molecular mechanism of ferroptosis has shed light on the current findings of ferroptosis-based nanodrug targeting strategies,such as driving ferroptosis in tumor cells and the tumor microenvironment,emerging combination therapy and against multidrug resistance.Furthermore,this review highlights the challenge and perspective of a ferroptosis-driven nanodrug delivery system for CRC-targeted therapy.

关键词： Colorectal cancer Ferroptosis Iron metabolism Lipid metabolism Nano delivery system Immunotherapy

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Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

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Science china(Life Sciences) 2023年第12期66卷 2786-2804页

作者： Shuting Yu ZhiYong Sun Xiuzhu Wang Tiantian Ju Changhao Wang Yingqi Liu Zhezhe Qu KuiWu Liu Zhongting Mei Na Li Meixi Lu Fan Wu Min Huang Xiaochen Pang Yingqiong Jia Ying Li Yaozhi Zhang Shunkang Dou Jianhao Jiang Xin Li Baofeng Yang Weijie Du Department of Pharmacology(The State-Province Key Laboratories of Biomedicine Pharmaceutics of china Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China Northern Translational Medicine research and Cooperation Center Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150081China research Unit of Noninfectious Chronic Diseases in Frigid Zone Chinese Academy of Medical Sciences2019RU070Harbin 150081China Traditional Chinese Medicine School Beijing University of Chinese MedicineBeijing 100029China

Ischemic heart failure(HF)remains a leading cause of morbidity and mortality.Maintaining homeostasis of cardiac function and preventing cardiac remodeling deterioration are critical to halting HF progression.Methyltransferase-like protein 13(Mettl13)has been shown to regulate protein translation efficiency by acting as a protein lysine methyltransferase,but its role in cardiac pathology remains unexplored.This study aims to characterize the roles and mechanisms of Mettl13 in cardiac contractile function and HF.We found that Mettl13 was downregulated in the failing hearts of mice post-myocardial infarction(MI)and in a cellular model of oxidative stress.Cardiomyocyte-specific overexpression of Mettl13 mediated by AAV9-Mettl13 attenuated cardiac contractile dysfunction and fibrosis in response to MI,while silencing of Mettl13 impaired cardiac function in normal mice.Moreover,Mettl13 overexpression abrogated the reduction in cell shortening,Ca^(2+)transient amplitude and SERCA2a protein levels in the cardiomyocytes of adult mice with MI.Conversely,knockdown of Mettl13 impaired the contractility of cardiomyocytes,and decreased Ca^(2+)transient amplitude and SERCA2a protein expression in vivo and in vitro.Mechanistically,Mettl13 impaired the stability of c-Cbl by inducing lysine methylation of c-Cbl,which in turn inhibited ubiquitination-dependent degradation of SERCA2a.Furthermore,the inhibitory effects of knocking down Mettl13 on SERCA2a protein expression and Ca^(2+)transients were partially rescued by silencing c-Cbl in H_(2)O_(2)-treated cardiomyocytes.In conclusion,our study uncovers a novel mechanism that involves the Mettl13/c-Cbl/SERCA2a axis in regulating cardiac contractile function and remodeling,and identifies Mettl13 as a novel therapeutic target for ischemic HF.

关键词： heart failure Mettl13 SERCA2a c-Cbl ubiquitination

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Nanoparticle-mediated synergistic anticancer effect of ferroptosis and photodynamic therapy:Novel insights and perspectives

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Asian Journal of Pharmaceutical Sciences 2023年第4期18卷 22-44页

作者： Haiying Wang Chu Qiao Qiutong Guan Minjie Wei Zhenhua Li School of Pharmacy China Medical UniversityShenyang 110122China

Current antitumor monotherapy has many limitations,highlighting the need for novel synergistic anticancer strategies.Ferroptosis is an iron-dependent form of nonapoptotic cell death that plays a pivotal regulatory role in tumorigenesis and treatment.Photodynamic therapy(PDT)causes irreversible chemical damage to target lesions and is widely used in antitumor therapy.However,PDT’s effectiveness is usually hindered by several obstacles,such as hypoxia,excess glutathione(GSH),and tumor resistance.Ferroptosis improves the anticancer efficacy of PDT by increasing oxygen and reactive oxygen species(ROS)or reducing GSH levels,and PDT also enhances ferroptosis induction due to the ROS effect in the tumor microenvironment(TME).Strategies based on nanoparticles(NPs)can subtly exploit the potential synergy of ferroptosis and PDT.This review explores recent advances and current challenges in the landscape of the underlyingmechanisms regulating ferroptosis and PDT,as well as nano delivery system-mediated synergistic anticancer activity.These include polymers,biomimetic materials,metal organic frameworks(MOFs),inorganics,and carrier-free NPs.Finally,we highlight future perspectives of this novel emerging paradigm in targeted cancer therapies.

关键词： Nanoparticles Ferroptosis Photodynamic therapy Synergistic anticancer therapy Reactive oxygen species

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FAR591 promotes the pathogenesis and progression of SONFH by regulating Fos expression to mediate the apoptosis of bone microvascular endothelial cells

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Bone research 2023年第2期11卷 398-415页

作者： Fei Zhang Lei Wei Lei Wang Tao Wang Zhihong Xie Hong Luo Fanchao Li Jian Zhang Wentao Dong Gang Liu Qinglin Kang Xuesong Zhu Wuxun Peng Department of Emergency Orthopedics The Affiliated Hospital of Guizhou Medical UniversityGuiyangGuizhou550004China School of Clinical Medicine Guizhou Medical UniversityGuiyangGuizhou 550004China Department of Orthopedics Rhode Island HospitalBrown UniversityProvidenceRhode Island02903USA Department of Orthopedics Shanghai Jiao Tong University Affiliated Sixth People's HospitalShanghai 200233China Department of Orthopedics The First Affiliated Hospital of Soochow UniversitySuzhouJiangsu215000China

The specific pathogenesis of steroid-induced osteonecrosis of the femoral head(SONFH)is still not fully understood,and there is currently no effective early cure.Understanding the role and mechanism of long noncoding RNAs(lnc RNAs)in the pathogenesis of SONFH will help reveal the pathogenesis of SONFH and provide new targets for its early prevention and treatment.In this study,we first confirmed that glucocorticoid(GC)-induced apoptosis of bone microvascular endothelial cells(BMECs)is a pre-event in the pathogenesis and progression of SONFH.Then,we identified a new lnc RNA in BMECs via lnc RNA/m RNA microarray,termed Fosassociated linc RNA ENSRNOT00000088059.1(FAR591).FAR591 is highly expressed during GC-induced BMEC apoptosis and femoral head necrosis.Knockout of FAR591 effectively blocked the GC-induced apoptosis of BMECs,which then alleviated the damage of GCs to the femoral head microcirculation and inhibited the pathogenesis and progression of SONFH.In contrast,overexpression of FAR591 significantly promoted the GC-induced apoptosis of BMECs,which then aggravated the damage of GCs to the femoral head microcirculation and promoted the pathogenesis and progression of SONFH.Mechanistically,GCs activate the glucocorticoid receptor,which translocates to the nucleus and directly acts on the FAR591 gene promoter to induce FAR591 gene overexpression.Subsequently,FAR591 binds to the Fos gene promoter(–245–51)to form a stable RNA:DNA triplet structure and then recruits TATA-box binding protein associated factor 15 and RNA polymerase II to promote Fos expression through transcriptional activation.Fos activates the mitochondrial apoptotic pathway by regulating the expression of Bcl-2 interacting mediator of cell death(Bim)and P53 upregulated modulator of apoptosis(Puma)to mediate GC-induced apoptosis of BMECs,which leads to femoral head microcirculation dysfunction and femoral head necrosis.In conclusion,these results confirm the mechanistic link between lnc RNAs and the pathogenesis of SONFH,which helps reveal the path

关键词： pathogenesis prevention inhibited

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Efficacy of short-term multidisciplinary intensive rehabilitation in patients with different Parkinson's disease motor subtypes: a prospective pilot study with 3-month follow-up

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Neural Regeneration research 2021年第7期16卷 1336-1343页

作者： Ke-Ke Chen Zhao-Hui Jin Lei Gao Lin Qi Qiao-Xia Zhen Cui Liu Ping Wang Yong-Hong Liu Rui-Dan Wang Yan-Jun Liu Jin-Ping Fang Yuan Su Xiao-Yan Yan Ai-Xian Liu Bo-Yan Fang Beijing Rehabilitation medical College Capital Medical UniversityBeijingChina Parkinson medical Center Beijing Rehabilitation HospitalCapital Medical UniversityBeijingChina Peking university Clinical research Institute BeijingChina

Parkinson's disease(PD) can be classified into three motor-based subtypes: postural instability/gait difficulty(PIGD), tremor dominant(TD), and indeterminate.The neuropathophysiological mechanisms of the three motor subtypes are different, which may lead to different responses to therapy.Sixty-nine patients with idiopathic Parkinson's disease(Hoehn–Yahr stage ≤ 3) were screened from 436 patients with Parkinsonism recruited through outpatient services and the internet.According to the Movement Disorder Society Unified Parkinson's Disease Rating Scale(MDS-upDRS) TD/PIGD ratio, the patients were divided into PIGD(TD/PIGD ≤ 0.09;n = 36), TD(TD/PIGD ≥1.15;n = 19), and indeterminate(TD/PIGD = 0.90–1.15;n = 14) groups.All patients received 2 weeks of multidisciplinary intensive rehabilitation treatment(MIRT) during hospitalization, as well as a remote home rehabilitation health education class.Compared with the scores at admission, all patients showed significant improvements in their MDS-upDRS III score, walking ability, balance, and posture control at discharge.Moreover, the MDS-upDRS III score improvement was greater in the PIGD group than in the TD group.The follow-up data, collected for 3 months after discharge, showed that overall symptom improvement in each group was maintained for 1–3 months.Furthermore, there were no significant differences in the duration or grade effects of symptom improvement among the three groups.These findings suggest that 2 weeks of MIRT is effective for improving motor performance in all three motor subtypes.Patients in the PIGD group had a better response after hospitalization than those in the TD group.This study was approved by the Institutional Ethics Committee of Beijing Rehabilitation Hospital of Capital medical university of china(approval No.2018 bkky022) on May 7, 2018 and registered with the Chinese Clinical Trial Registry(registration No.Chi CTR1900020771) on January 19, 2019.

关键词： balance gait motor neurodegeneration Parkinson's disease posture rehabilitation tremor

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