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m^(6)A reader YTHDF1 promotes cardiac fibrosis by enhancing AXL translation

Frontiers of Medicine 2024年第3期18卷 499-515页

作者： Han Wu Weitao Jiang Ping Pang Wei Si Xue Kong Xinyue Zhang Yuting Xiong Chunlei Wang Feng Zhang Jinglun Song Yang Yang Linghua Zeng Kuiwu Liu Yingqiong Jia Zhuo Wang Jiaming Ju Hongtao Diao Yu Bian Baofeng Yang Department of Pharmacology(National Key Laboratory of Frigid Zone Cardiovascular Diseases the State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin150081China

cardiac fibrosis caused by ventricular remodeling and dysfunction such as post-myocardial infarction(MI)can lead to heart failure.RNA N6-methyladenosine(m^(6)A)methylation has been shown to play a pivotal role in the occurrence and development of many illnesses.In investigating the biological function of the m^(6)A reader YTHDF1 in cardiac fibrosis,adeno-associated virus 9 was used to knock down or overexpress the YTHDF1 gene in mouse hearts,and MI surgery in vivo and transforming growth factor-β(TGF-β)-activated cardiac fibroblasts in vitro were performed to establish fibrosis models.Our results demonstrated that silencing YTHDF1 in mouse hearts can significantly restore impaired cardiac function and attenuate myocardial fibrosis,whereas YTHDF1 overexpression could further enhance cardiac dysfunction and aggravate the occurrence of ventricular pathological remodeling and fibrotic development.Mechanistically,zinc finger BED-type containing 6 mediated the transcriptional function of the YTHDF1 gene promoter.YTHDF1 augmented AXL translation and activated the TGF-β-Smad2/3 signaling pathway,thereby aggravating the occurrence and development of cardiac dysfunction and myocardial fibrosis.Consistently,our data indicated that YTHDF1 was involved in activation,proliferation,and migration to participate in cardiac fibrosis in vitro.Our results revealed that YTHDF1 could serve as a potential therapeutic target for myocardial fibrosis.

关键词： cardiac fibrosis YTHDF1 AXL ZBED6 heart failure

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Notum protects against myocardial infarction-induced heart dysfunction by alleviating cardiac fibrosis

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Frigid Zone Medicine 2024年第1期4卷 41-50页

作者： Tongzhu Jin Zhen Ye Ruonan Fang Yue Li Wei Su Qianqian Wang Tianyu Li Hongli Shan Yanjie Lu Haihai Liang Laboratory of Frigid Zone Cardiovascular Diseases(SKLFZCD) Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China Department of Pharmacy Suqian First HospitalSuqian 223800China Research Unit of Noninfectious Chronic Diseases in Frigid Zone(2019RU070) Chinese Academy of Medical SciencesHarbin 150081China

Background and Objective:cardiac fibrosis is a pathological reparative process that follows myocardial infarctionand is associated with compromised cardiac systolic and reduced cardiac compliance.The Wnt signaling pathway is closely implicated in organ fibrosis,and Notum,a highly conserved secreted inhibitor,modulates Wnt signaling.The objective of this study was to explore the role and mechanism of Notum in cardiac fibrosis.Methods:A mouse model of cardiac remodeling was established through left coronary artery ligation surgery,with the addition of Notum injection following myocardial infarction surgery.The protective effect of Notum on myocardial infarction was assessed by evaluating cardiac function,including survival rate,echocardiographic assessment,and cardiac contraction analyses.Inflammatory cell necrosis and infiltration were confirmed through H&E and Masson staining.The expression of fibrosis-related genes andβ-catenin pathway markers was detected using Western blot quantificational RT-PCR(qRT-PCR).Additionally,EdU,wound healing,and immunofluorescence staining analyses were performed to detect the effect of Notum's in transforming growth factor beta-1(TGF-β1)induced myofibroblast transformation.Results:The administration of Notum treatment resulted in enhanced survival rates,improved cardiac function,and decreased necrosis and infiltration of inflammatory cells in mice subjected to left coronary artery ligation.Furthermore,Notum effectively impeded the senescence of cardiac fibroblasts and hindered their pathological transformation into cardiac fibroblasts.Additionally,it significantly reduced collagen production and attenuated the activation of the Wnt/β-catenin pathway.Our preliminary investigations successfully demonstrated the therapeutic potential of Notum in both fibroblasts in vitro and in a mouse model of myocardial infarction-induced cardiac fibrosis in vivo.Conclusion:Notum inhibition of the Wnt/β-catenin signaling pathway and cardiac fibroblast senescence ultimately hampers the onset of cardi

关键词： cardiac fibrosis Notum Wnt/β-catenin senescence myocardial infarction

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Exercise training attenuates angiotensinⅡ-induced cardiac fibrosis by reducing POU2F1 expression

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Journal of Sport and Health Science 2023年第4期12卷 464-476页

作者： Na Feng Haiyi Yu Yueshen Wang Youyi Zhang Han Xiao Wei Gao Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNational Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Research Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases Chinese Academy of Medical SciencesBeijing 100191China

Background:Exercise training protects against heart failure.However,the mechanism underlying the protective effect of exercise training on angiotensinⅡ(AngⅡ)-induced cardiac fibrosis remains unclear.Methods:An exercise model involving C57BL/6N mice and 6 weeks of treadmill training was used.AngⅡ(1.44 mg/kg/day)was administered to induce cardiac fibrosis.RNA sequencing and bioinformatic analysis were used to identify the key factors mediating the effects of exercise training on cardiac fibrosis.Primary adult mouse cardiac fibroblasts(CFs)were used in vitro.Adeno-associated virus serotype 9 was used to overexpress POU domain,class 2,transcription factor 1(POU2F1)in vivo.Results:Exercise training attenuated AngⅡ-induced cardiac fibrosis and reversed 39 gene expression changes.The transcription factor regulating the largest number of these genes was POU2F1.Compared to controls,POU2F1 was shown to be signififcantly upregulated by AngⅡ,which is itself reduced by exercise training.In vivo,POU2F1 overexpression nullified the benefits of exercise training on cardiac fibrosis.In CFs,POU2F1 promoted cardiac fibrosis.CCAAT enhancer-binding proteinβ(C/EBPβ)was predicted to be the transcription factor of POU2F1and verified using a dual-luciferase reporter assay.In vivo,exercise training activated AMP-activated protein kinase(AMPK)and alleviated the increase in C/EBPβinduced by AngⅡ.In CFs,AMPK agonist inhibited the increase in C/EBPβand POU2F1 induced by Ang II,whereas AMPK inhibitor reversed this effect.Conclusion:Exercise training attenuates AngⅡ-induced cardiac fibrosis by reducing POU2F1.Exercise training inhibits POU2F1 by activating AMPK,which is followed by the downregulation of C/EBPβ,the transcription factor of POU2F1.

关键词： AMPK C/EBPβ cardiac fibrosis Exercise POU2F1

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Discovery of novel 4-phenylquinazoline-based BRD4 inhibitors for cardiac fibrosis

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Acta Pharmaceutica Sinica B 2022年第1期12卷 291-307页

作者： Zhangxu He Haomiao Jiao Qi An Xin Zhang Dan Zengyangzong Jiale Xu Hongmin Liu Liying Ma Wen Zhao State Key Laboratory of Esophageal Cancer Prevention and Treatment Key Laboratory of Advanced Pharmaceutical TechnologyMinistry of Education of ChinaSchool of Pharmaceutical SciencesZhengzhou UniversityZhenzhou 450001China China Meheco Topfond Pharmaceutical Co. Zhumadian 463000China

Bromodomain containing protein 4(BRD4), as an epigenetic reader, can specifically bind to the acetyl lysine residues of histones and has emerged as an attractive therapeutic target for various diseases,including cancer, cardiac remodeling and heart failure. Herein, we described the discovery of hit 5 bearing4-phenylquinazoline skeleton through a high-throughput virtual screen using 2,003,400 compound library(enamine). Then, structure-activity relationship(SAR) study was performed and 47 new 4-phenylquinazoline derivatives toward BRD4 were further designed, synthesized and evaluated, using HTRF assay set up in our lab. Eventually, we identified compound C-34, which possessed better pharmacokinetic and physicochemical properties as well as lower cytotoxicity against NRCF and NRCM cells, compared to the positive control JQ1. Using computer-based molecular docking and cellular thermal shift assay, we further verified that C-34 could target BRD4 at molecular and cellular levels. Furthermore, treatment with C-34 effectively alleviated fibroblast activation in vitro and cardiac fibrosis in vivo, which was correlated with the decreased expression of BRD4 downstream target c-MYC as well as the depressed TGF-β1/Smad2/3 signaling pathway.Taken together, our findings indicate that novel BRD4 inhibitor C-34 tethering a 4-phenylquinazoline scaffold can serve as a lead compound for further development to treat fibrotic cardiovascular disease.

关键词： BRD4 Inhibitor 4-Phenylquinazoline cardiac fibrosis

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LncRNA CFAR promotes cardiac fibrosis via the miR-449a-5p/LOXL3/mTOR axis

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Science China(Life Sciences) 2023年第4期66卷 783-799页

作者： Mingyu Zhang Bowen Zhang Xiaohan Wang Jiahang Song Ming Tong Zheng Dong Jiaonan Xu Meng Liu Yuan Jiang Ning Wang Ying Wang Zhimin Du Yanyan Liu Rong Zhang Chaoqian Xu Department of Pharmacology State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular Medicine ResearchMinistry of EducationCollege of PharmacyHarbin Medical UniversityHarbin 150081China Department of Pharmacy The Second Affiliated Hospital of Harbin Medical UniversityHarbin 150081China Institute of Clinical Pharmacy The Second Affiliated Hospital of Harbin Medical UniversityHarbin 150081China Zhuhai People’s Hospital Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and TreatmentZhuhai Hospital Affiliated with Jinan UniversityJinan UniversityZhuhai 519000China Center of Chronic Diseases and Drug Research of Mudanjiang Medical University Mudanjiang 157011China

cardiac fibrosis is one of the crucial pathological factors in the heart,and various cardiac conditions associated with excessive fibrosis can eventually lead to heart failure.However,the exact molecular mechanism of cardiac fibrosis remains unclear.In the present study,we show that a novel lnc RNA that we named cardiac fibrosis-associated regulator(CFAR)is a profibrotic factor in the heart.CFAR was upregulated in cardiac fibrosis and its knockdown attenuated the expression of fibrotic marker genes and the proliferation of cardiac fibroblasts,thereby ameliorating cardiac fibrosis.Moreover,CFAR acted as a ce RNA sponge for mi R-449a-5p and derepressed the expression of LOXL3,which we experimentally established as a target gene of mi R-449a-5p.In contrast to CFAR,mi R-449a-5p was found to be significantly downregulated in cardiac fibrosis,and artificial knockdown of mi R-449a-5p exacerbated fibrogenesis,whereas overexpression of mi R-449a-5p impeded fibrogenesis.Furthermore,we found that LOXL3 mimicked the fibrotic factor TGF-β1 to promote cardiac fibrosis by activating m TOR.Collectively,our study established CFAR as a new profibrotic factor acting through a novel mi R-449a-5p/LOXL3/m TOR axis in the heart and therefore might be considered as a potential molecular target for the treatment of cardiac fibrosis and associated heart diseases.

关键词： CFAR miR-449a-5p LOXL3 mTOR cardiac fibrosis

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Cytokine receptor-like factor 1(CRLF1)promotes cardiac fibrosis via ERK1/2 signaling pathway

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第8期24卷 682-697页

作者： Shenjian LUO Zhi YANG Ruxin CHEN Danming YOU Fei TENG Youwen YUAN Wenhui LIU Jin LI Huijie ZHANG Department of Endocrinology and Metabolism Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Guangdong Provincial Key Laboratory of Shock and Microcirculation Southern Medical UniversityGuangzhou 510515China State Key Laboratory of Organ Failure Research Nanfang HospitalSouthern Medical UniversityGuangzhou 510515China Department of Endocrinology Shanxi Medical University Affiliated Second HospitalTaiyuan 030001China

cardiac fibrosis is a cause of morbidity and mortality in people with heart disease.Anti-fibrosis treatment is a significant therapy for heart disease,but there is still no thorough understanding of fibrotic mechanisms.This study was carried out to ascertain the functions of cytokine receptor-like factor 1(CRLF1)in cardiac fibrosis and clarify its regulatory mechanisms.We found that CRLF1 was expressed predominantly in cardiac fibroblasts.Its expression was up-regulated not only in a mouse heart fibrotic model induced by myocardial infarction,but also in mouse and human cardiac fibroblasts provoked by transforming growth factor-β1(TGF-β1).Gain-and loss-of-function experiments of CRLF1 were carried out in neonatal mice cardiac fibroblasts(NMCFs)with or without TGF-β1 stimulation.CRLF1 overexpression increased cell viability,collagen production,cell proliferation capacity,and myofibroblast transformation of NMCFs with or without TGF-β1 stimulation,while silencing of CRLF1 had the opposite effects.An inhibitor of the extracellular signal-regulated kinase 1/2(ERK1/2)signaling pathway and different inhibitors of TGF-β1 signaling cascades,comprising mothers against decapentaplegic homolog(SMAD)-dependent and SMAD-independent pathways,were applied to investigate the mechanisms involved.CRLF1 exerted its functions by activating the ERK1/2 signaling pathway.Furthermore,the SMAD-dependent pathway,not the SMAD-independent pathway,was responsible for CRLF1 up-regulation in NMCFs treated with TGF-β1.In summary,activation of the TGF-β1/SMAD signaling pathway in cardiac fibrosis increased CRLF1 expression.CRLF1 then aggravated cardiac fibrosis by activating the ERK1/2 signaling pathway.CRLF1 could become a novel potential target for intervention and remedy of cardiac fibrosis.

关键词： Cytokine receptor-like factor 1(CRLF1) TGF-β1/SMAD signaling pathway ERK1/2 signaling pathway cardiac fibrosis Myofibroblast transformation Extracellular matrix(ECM)

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cardiac fibroblast heat shock protein 47 aggravates cardiac fibrosis post myocardial ischemia-reperfusion injury by encouraging ubiquitin specific peptidase 10 dependent Smad4 deubiquitination

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Acta Pharmaceutica Sinica B 2022年第11期12卷 4138-4153页

作者： Saiyang Xie Yun Xing Wenke Shi Min Zhang Mengya Chen Wenxi Fang Shiqiang Liu Tong Zhang Xiaofeng Zeng Si Chen Shasha Wang Wei Deng Qizhu Tang Department of Cardiology Renmin Hospital of Wuhan UniversityWuhan 430060China Hubei Key Laboratory of Metabolic and Chronic Diseases Wuhan 430060China Cardiovascular Research Institute of Wuhan University Wthan 430060China

Despite complications were significantly reduced due to the popularity of percutaneous coronary intervention(PCI) in clinical trials, reperfusion injury and chronic cardiac remodeling significantly contribute to poor prognosis and rehabilitation in AMI patients. We revealed the effects of HSP47 on myocardial ischemia-reperfusion injury(IRI) and shed light on the underlying molecular mechanism.We generated adult mice with lentivirus-mediated or miRNA(mi1/133TS)-aided cardiac fibroblastselective HSP47 overexpression. Myocardial IRI was induced by 45-min occlusion of the left anterior descending(LAD) artery followed by 24 h reperfusion in mice, while ischemia-mediated cardiac remodeling was induced by four weeks of reperfusion. Also, the role of HSP47 in fibrogenesis was evaluated in cardiac fibroblasts following hypoxia-reoxygenation(HR). Extensive HSP47 was observed in murine infarcted hearts, human ischemic hearts, and cardiac fibroblasts and accelerated oxidative stress and apoptosis after myocardial IRI. cardiac fibroblast-selective HSP47 overexpression exacerbated cardiac dysfunction caused by chronic myocardial IRI and presented deteriorative fibrosis and cell proliferation.HSP47 upregulation in cardiac fibroblasts promoted TGFβ1-Smad4 pathway activation and Smad4 deubiquitination by recruiting ubiquitin-specific peptidase 10(USP10) in fibroblasts. However, cardiac fibroblast specific USP10 deficiency abolished HSP47-mediated fibrogenesis in hearts. Moreover, blockage of HSP47 with Col003 disturbed fibrogenesis in fibroblasts following HR. Altogether, cardiac fibroblast HSP47 aggravates fibrosis post-myocardial IRI by enhancing USP10-dependent Smad4 deubiquitination,which provided a potential strategy for myocardial IRI and cardiac remodeling.

关键词： Heat shock protein 47 Myocardial ischemia-reperfusion injury Ubiquitin-specific protease 10 cardiac fibrosis s Smad4 Fibroblast Cell proliferation Cardiae dysfunction

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cardiac fibrosis: Histological features, molecular pathways and therapeutic targets

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South China Journal of Cardiology 2022年第2期23卷 115-128页

作者：孙建建钟涛朱平 Department of cardiac Surgery and Department of Medical Research CenterGuangdong Cardiovascular InstituteGuangdong Provincial People's HospitalGuangdong Academy of Medical SciencesGuangdong Provincial Key Laboratory of PathogenesisTargeted Prevention and Treatment of Heart DiseaseGuangzhouGuangdong 510080China Shanghai Key Laboratory of Regulatory Biology Institute of Molecular MedicineEast China Normal UniversitySchool of Life Sciences200241ShanghaiP.R.China

cardiac fibrosis is defined as the unbalanced production and degradation of cardiac interstitial extracellular matrix(ECM),leading to systolic and diastolic dysfunction,arrhythmias,and adverse outcomes of many cardiac pathophysiological conditions.The accumulation of myocardial ECM increases the risk of arrhythmias and impairs cardiac function,ultimately leading to the development of heart failure.Although slowing or reversing the development of excessive accumulation of ECM and cardiac fibrosis is important for maintaining cardiac function,there is currently no approved treatment for them.Activated cardiac fibroblasts are the main effector cells of cardiac fibrosis.Their expansion after pathophysiologic stimuli such as pressure overload,volume overload,metabolic dysfunction,wound healing,and aging is primarily driven by activating resident interstitial populations.While cardiac fibroblasts are the primary effector cells in the fibrotic heart,monocytes/macrophages,lymphocytes,mast cells,vascular cells,and cardiomyocytes may also contribute to the fibrotic response,by secreting critical fibrotic factors and matricellular proteins.This review discusses histological features,molecular pathways involved in the pathogenesis of cardiac fibrosis and possible therapeutic targets.Understanding the occurrence,development and diffusion mechanisms of cardiac fibrosis has important clinical implications for the discovery of drugs to prevent the progression of cardiac fibrosis.

关键词： cardiac fibrosis ECM cardiac fibroblasts Histological features Molecular pathways

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Chronic inhibition of cyclic guanosine monophosphate-specific phosphodiesterase 5 prevented cardiac fibrosis through inhibi- tion of transforming growth factor 13-induced Smad signaling

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Frontiers of Medicine 2014年第4期8卷 445-455页

作者： Wei Gong＊ Mengwen Yan Junxiong Chen Sandip Chaugai Chen Chen Daowen Wang Department of Internal Medicine and Gene Therapy Center Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Recent evidences suggested that cyclic guanosine monophosphate-specific phosphodiesterase 5 （PDE5） inhibitor represents an important therapeutic target for cardiovascular diseases. Whether and how it ameliorates cardiac fibrosis, a major cause of diastolic dysfunction and heart failure, is unknown. The purpose of this study was to investigate the effects of PDE5 inhibitor on cardiac fibrosis. We assessed cardiac fibrosis and pathology in mice subjected to transverse aortic constriction （TAC）. Oral sildenafil, a PDE5 inhibitor, was administered in the therapy group. In control mice, 4 weeks of TAC induced significant cardiac dysfunction, cardiac fibrosis, and cardiac fibroblast activation （proliferation and transformation to myofibroblasts）. Sildenafil treatment markedly prevented TAC-induced cardiac dysfunction, cardiac fibrosis and cardiac fibroblast activation but did not block TAC-induced transforming growth factor-β0 （TGF-β1） production and phosphorylation of Smad2/3. In isolated cardiac fibroblasts, sildenafil blocked TGF-β1-induced cardiac fibroblast transformation, proliferation and collagen synthesis. Furthermore, we found that sildenafil induced phosphorylated cAMP response element binding protein （CREB） and reduced CREB-binding protein 1 （CBP1） recruitment to Smad transcriptional complexes. PDE5 inhibition prevents cardiac fibrosis by reducing CBP1 recruitment to Smad transcriptional complexes through CREB activation in cardiac fibroblasts.

关键词： PDE5 cardiac fibrosis TGF-β CREB

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Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2021年第10期22卷 818-838页

作者： Kun ZHAO Jing ZHANG Tianhua XU Chuanxi YANG LiqingWENG TingtingWU XiaoguangWU Jiaming MIAO Xiasheng GUO Juan TU Dong ZHANG Bin ZHOU Wei SUN Xiangqing KONG Department of Cardiology the First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029China Key Laboratory of Modern Acoustics Department of PhysicsCollaborative Innovation Center of Advanced MicrostructureNanjing UniversityNanjing 210093China Departments of Genetics Pediatricsand Medicine(Cardiology)Wilf Cardiovascular Research InstituteAlbert Einstein College of MedicineBronxNY 10461USA

Objective:cardiac hypertrophy and fibrosis are major pathological manifestations observed in left ventricular remodeling induced by angiotensin II(AngII).Low-intensity pulsed ultrasound(LIPUS)has been reported to ameliorate cardiac dysfunction and myocardial fibrosis in myocardial infarction(MI)through mechano-transduction and its downstream pathways.In this study,we aimed to investigate whether LIPUS could exert a protective effect by ameliorating AngII-induced cardiac hypertrophy and fibrosis and if so,to further elucidate the underlying molecular mechanisms.Methods:We used AngII to mimic animal and cell culture models of cardiac hypertrophy and fibrosis.LIPUS irradiation was applied in vivo for 20 min every 2 d from one week before mini-pump implantation to four weeks after mini-pump implantation,and in vitro for 20 min on each of two occasions 6 h apart.cardiac hypertrophy and fibrosis levels were then evaluated by echocardiographic,histopathological,and molecular biological methods.Results:Our results showed that LIPUS could ameliorate left ventricular remodeling in vivo and cardiac fibrosis in vitro by reducing AngII-induced release of inflammatory cytokines,but the protective effects on cardiac hypertrophy were limited in vitro.Given that LIPUS increased the expression of caveolin-1 in response to mechanical stimulation,we inhibited caveolin-1 activity with pyrazolopyrimidine 2(pp2)in vivo and in vitro.LIPUS-induced downregulation of inflammation was reversed and the anti-fibrotic effects of LIPUS were absent.Conclusions:These results indicated that LIPUS could ameliorate AngII-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway,providing new insights for the development of novel therapeutic apparatus in clinical practice.

关键词： Low-intensity pulsed ultrasound(LIPUS) Caveolin-1 cardiac fibrosis Inflammation Angiotensin II(AngII)

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