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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 *** N6-methyladenosine(m^(6)A)methylation has been shown to play a pivotal role in the occurrence and development of many *** 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 *** 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 ***,zinc finger BED-type containing 6 mediated the transcriptional function of the YTHDF1 gene ***1 augmented AXL translation and activated the TGF-β-Smad2/3 signaling pathway,thereby aggravating the occurrence and development of cardiac dysfunction and myocardial ***,our data indicated that YTHDF1 was involved in activation,proliferation,and migration to participate in cardiac fibrosis in *** 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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Buxu Tongyu Granule Alleviates Myocardial Ischemia by Activating Vascular Smooth Muscle Cell Soluble Guanylate Cyclase to Inhibit Abnormal Vasomotion

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Engineering 2024年第7期38卷 133-143页

作者： Shuang Yang Yixiu Zhao Xiaoling Cheng Tingting Zhan Jiaying Tian Xue Liu Chunyue Ma Zhiqi Wang Luying Jin Qian Liu Yanli Wang Jian Huang Jinhui Wang Yan Zhang Baofeng Yang Department of Pharmacology&key laboratory of cardiovascular Medicine Research Ministry of Education of the People’s Republic of ChinaCollege of PharmacyHarbin Medical UniversityHarbin 150081China national key laboratory of frigid zone cardiovascular diseases(NKLFZCD) Harbin Medical UniversityHarbin 150081China Department of Medicinal Chemistry and Natural Medicine Chemistry College of PharmacyHarbin Medical UniversityHarbin 150081China Research Unit of Noninfectious Chronic diseases in frigid zones Chinese Academy of Medical SciencesHarbin 150081China

Myocardial ischemia is a serious threat to human health,and vascular dysfunction is its main *** Tongyu(BXTY)Granule is an effective traditional Chinese medicine(TCM)for treating myocardial ***,the underlying mechanism of BXTY is still *** this study,we demonstrate that BXTY ameliorates myocardial ischemia by activating the soluble guanylate cyclase(sGC)-30,50-cyclic guanosine monophosphate(cGMP)-protein kinase G(PKG)signaling pathway in vascular smooth muscle cells(VSMCs)to dilate the *** was given by gavage for ten consecutive days before establishing an animal model of acute myocardial ischemia in mice via the intraperitoneal injection of *** results showed that BXTY alleviated the symptoms of myocardial ischemia induced by pituitrin in mice,including electrocardiogram abnormalities and changes in plasma *** addition,BXTY dilated pre-constricted blood vessels and inhibited the vasoconstriction of the superior mesenteric artery in a dose-dependent but endothelial-independent *** effects were eliminated by preincubating vascular rings with the sGC inhibitors NS 2028 or ODQ,or with the PKG inhibitor KT ***,BXTY increased the protein expression of sGC-b1 and the intracellular second messenger cGMP level in mouse aortic vascular smooth muscle cells(MOVAs).NS 2028 or ODQ reversed these effects of *** expression level of the cGMP downstream effector protein PKG-1 increased after treating MOVAs with *** 2028,ODQ,or KT 5823 also reversed this effect of *** conclusion,BXTY can improve the symptoms of acute myocardial ischemia in mice,and activating the sGC-cGMP-PKG pathway in VSMCs to induce vasodilation is its key pharmacodynamic mechanism.

关键词： Myocardial ischemia Vasomotion Soluble guanylate cyclase Buxu Tongyu Granule

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LncRNA CCRR maintains Ca^(2+)homeostasis against myocardial infarction through the FTO-SERCA2a pathway

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Science China(Life Sciences) 2024年第8期67卷 1601-1619页

作者： Hua Yang Lina Xuan Shengjie Wang Huishan Luo Xiaomeng Duan Jianjun Guo Shijia Cui Jieru Xin Junwei Hao Xiufang Li Jun Chen Feihan Sun Xiaolin Hu Siyun Li Ying Zhang Lei Jiao Baofeng Yang Lihua Sun Department of Pharmacology Harbin Medical University(State Key Laboratory of Frigid Zone Cardiovascular Diseasethe State-Province Key Laboratories of Biomedicine-Pharmaceutics of ChinaKey Laboratory of Cardiovascular ResearchMinistry of EducationJoint International Research Laboratory of Cardiovascular Medicine ResearchMinistry of EducationChina)College of PharmacyHarbin Medical UniversityHarbin 150081China

Cardiac conduction regulatory RNA(CCRR)has been documented as an antiarrhythmic lncRNA in our earlier *** study aimed to evaluate the effects of CCRR on SERCA2a and the associated Ca^(2+)homeostasis in myocardial infarction(MI).Overexpression of CCRR via AAV9-mediated delivery not only partially reversed ischemia-induced contractile dysfunction but also alleviated abnormal Ca^(2+)homeostasis and reduced the heightened methylation level of SERCA2a following *** effects were also observed in CCRR overexpressing transgenic mice.A conserved sequence domain of CCRR mimicked the protective function observed with the full ***,silencing CCRR in healthy mice led to intracellular Ca^(2+)overloading of *** increased SERCA2a protein stability by upregulating FTO *** direct interaction between CCRR and FTO protein was characterized by RNA-binding protein immunoprecipitation(RIP)analysis and RNA pulldown *** of NFATc3 was identified as an upstream mechanism responsible for CCRR downregulation in *** study demonstrates that CCRR is a protective lncRNA that acts by maintaining the function of FTO,thereby reducing the m^(6)A RNA methylation level of SERCA2a,ultimately preserving calcium homeostasis for myocardial contractile function in ***,CCRR may be considered a promising therapeutic strategy with a beneficial role in cardiac pathology.

关键词： CCRR calcium homeostasis FTO myocardial infarction SERCA2a

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ASF1A-dependent P300-mediated histone H3 lysine 18 lactylation promotes atherosclerosis by regulating EndMT

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Acta Pharmaceutica Sinica B 2024年第7期14卷 3027-3048页

作者： Mengdie Dong Yunjia Zhang Minghong Chen Yongkang Tan Jiao Min Xian He Fuhao Liu Jiaming Gu Hong Jiang Longbin Zheng Jiajing Chen Quanwen Yin Xuesong Li Xiang Chen Yongfeng Shao Yong Ji Hongshan Chen Department of cardiovascular Surgery the First Affiliated Hospital of Nanjing Medical Universityand Key Laboratory of Cardiovascular and Cerebrovascular MedicineSchool of PharmacyNational Vaccine Innovation PlatformNanjing Medical UniversityNanjing 211166China key laboratory of cardiovascular and Cerebrovascular Medicine School of PharmacyNanjing Medical UniversityNanjing 211166China Department of Clinical Medicine Nanjing Medical University TIANYUAN Honors SchoolNanjing Medical UniversityNanjing 211166China Department of Anesthesiology Sir Run Run HospitalNanjing Medical UniversityNanjing 211166China Department of cardiovascular Surgery the First Affiliated Hospital of Nanjing Medical UniversityNanjing 211166China key laboratory of cardiovascular and Cerebrovascular Medicine Key Laboratory of Targeted Intervention of Cardiovascular DiseaseCollaborative Innovation Center for Cardiovascular Disease Translational MedicineState Key Laboratory of Reproductive MedicineSchool of Pharmacythe Affiliated Suzhou Hospital of Nanjing Medical UniversityGusu SchoolNanjing Medical UniversityNanjing 211166China national key laboratory of frigid zone cardiovascular diseases(NKLFZCD) Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China)College of PharmacyKey Laboratory of Cardiovascular Medicine Research and Key Laboratory of Myocardial IschemiaChinese Ministry of EducationNHC Key Laboratory of Cell Transplantationthe Central Laboratory of the First Affiliated HospitalHarbin Medical UniversityHarbin 150081China key laboratory of Targeted Intervention of cardiovascular Disease Collaborative Innovation Center for Cardiovascular Disease Translational MedicineNanjing Medical UniversityNanjing 211166China Department of Cardiology Huai’an First People’s Hospital Affiliated with Nanjing Medical UniversityHuai’an 223399China

Endothelial-to-mesenchymal transition(EndMT)is a key driver of *** glycolysis is increased in the endothelium of atheroprone areas,accompanied by elevated lactate *** lactylation,mediated by lactate,can regulate gene expression and participate in disease ***,whether histone lactylation is involved in atherosclerosis remains ***,we report that lipid peroxidation could lead to EndMT-induced atherosclerosis by increasing lactatedependent histone H3 lysine 18 lactylation(H3K18la)in vitro and in vivo,as well as in atherosclerotic patients’***,the histone chaperone ASF1A was first identified as a cofactor of P300,which precisely regulated the enrichment of H3K18la at the promoter of SNAI1,thereby activating SNAI1 transcription and promoting *** found that deletion of ASF1A inhibited EndMT and improved endothelial *** analysis based on Apoe^(KO)Asf1a^(ECKO) mice in the atherosclerosis model confirmed the involvement of H3K18la in atherosclerosis and found that endotheliumspecific ASF1A deficiency inhibited EndMT and alleviated atherosclerosis *** of glycolysis by pharmacologic inhibition and advanced PROTAC attenuated H3K18la,SNAI1 transcription,and EndMT-induced *** study illustrates precise crosstalk between metabolism and epigenetics via H3K18la by the P300/ASF1A molecular complex during EndMT-induced atherogenesis,which provides emerging therapies for atherosclerosis.

关键词： Histone lactylation Atherosclerosis Endothelial-tomesenchymal transition ASF1A SNAI1 Endothelial dysfunction Lactate Epigenetic

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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 *** Wnt signaling pathway is closely implicated in organ fibrosis,and Notum,a highly conserved secreted inhibitor,modulates Wnt *** objective of this study was to explore the role and mechanism of Notum in cardiac ***:A mouse model of cardiac remodeling was established through left coronary artery ligation surgery,with the addition of Notum injection following myocardial infarction *** protective effect of Notum on myocardial infarction was assessed by evaluating cardiac function,including survival rate,echocardiographic assessment,and cardiac contraction *** cell necrosis and infiltration were confirmed through H&E and Masson *** 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 ***: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 ***,Notum effectively impeded the senescence of cardiac fibroblasts and hindered their pathological transformation into cardiac ***,it significantly reduced collagen production and attenuated the activation of the Wnt/β-catenin *** 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 ***:Notum inhibition of the Wnt/β-catenin signaling pathway and cardiac fibroblast

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

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Peroxisome proliferator-activated receptors gama ameliorates liver fibrosis in non-alcoholic fatty liver disease by inhibiting TGF-β/Smad signaling activation

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frigid zone Medicine 2024年第1期4卷 12-22页

作者： Qingwei Zhang Wenjie Zhao Zeqi Sun Xinxin Dong Liwei Zhu Zhen Zhang Ximing Chen Yingying Hu Menghan Du Jiamin Li Yong Zhang Department of Pharmacology College of Pharmacyand Department of Cardiologythe Second Affiliated HospitalHarbin Medical UniversityHarbin 150081China Department of Pharmacology College of PharmacyHarbin Medical UniversityHarbin 150081China The State key laboratory of frigid zone cardiovascular diseases(SKLFZCD) and the Key Laboratory of Cardiovascular Medicine ResearchMinistry of EducationHarbin 150081China Research Unit of Noninfectious Chronic diseases in frigid zone Chinese Academy of Medical Sciences2019RU070Harbin 150081China

Background:Nonalcoholic fatty liver disease(NAFLD)is a chronic condition characterized by a progressive decline in liver function,leading to disruptions in liver integrity and metabolic function,resulting in lipid deposition and excessive accumulation of extracellular matrix(ECM).The pathogenesis of NAFLD is complex and not yet fully understood,contributing to the absence of specific therapeutic *** proliferator-activated receptor gamma(PPARγ)is a ligand-activated transcription factor pivotal in regulating lipid and glucose ***,the impacts of PPARγon NAFLD remains insufficiently ***,this study aimed to investigate the role of PPARγin NAFLD and its underlying molecular ***:Chemical detection kits were utilized to quantify collagen content,alanine aminotransferase(ALT),and aspartate aminotransferase(AST)level *** real-time polymerase chain reaction(qRT-PCR)was employed to assess alterations in extracellular matrix-related genes and inflammatory response genes in liver tissue and HepG2 cells,while western blotting was conducted to analyze the levels of both PPARγand the TGF-β/Smad signaling ***:Our findings unveiled significantly reduced PPARγexpression in a rat model of NAFLD,leading to subsequent activation of the TGF-β/Smad signaling ***,PPARγactivation effectively mitigated NAFLD progression by inhibiting inflammation and fibrosis-related gene expression and collagen *** a cellular level,PPARγactivation was found to inhibit the expression of extracellular matrix-related genes such as matrix metalloproteinase 2(MMP2)and matrix metalloproteinase 9(MMP9),along with inflammatory response genes interleukin(IL)-1βand ***,PPARγactivation led to a significant decrease in the levels of ALT and *** the molecular level,PPARγnotably down-regulated the TGF-β/Smad signaling pathway,which is known to promote liver ***:These groundbre

关键词： NAFLD PPARγ TGF-β/Smad liver fibrosis

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Lipid-lowering effects of gefarnate in statin-treated patients with residual hypertriglyceridemia: a randomized controlled study

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Journal of Geriatric Cardiology 2024年第08期 791-798页

作者： Jing SHI Ming-Lu XU Mei-Jiao HE Wan-Lan BO Hai-Yu ZHANG Dang-Hui SUN Ding-Yu WANG Xiao-Yu WANG Qun SHAO Yu-Jiao PAN Yu ZHANG Chen-Guang DAI Jing-Ying WANG Lin-Wei ZHANG Guang-Zhong LIU Yue LI for the GPROT Study Group Department of Cardiology the First Affiliated Hospital Harbin Medical University Department of Gastroenterology the Fourth Affiliated Hospital Harbin Medical University Department of Cardiology Harbin Medical University Cancer Hospital Department of Cardiology Shenzhen People's Hospital national key laboratory of frigid zone cardiovascular diseases Harbin Medical University NHC key laboratory of Cell Transplantation Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province Heilongjiang Province Clinical Medical Research Center for Hypertension the First Affiliated Hospital Harbin Medical University Institute of Metabolic Disease Heilongjiang Academy of Medical Science

BACKGROUND The prevention of coronary artery disease (CAD) faces dual challenges:the aspirin-induced gastrointestinal injury,and the residual cardiovascular risk after statin *** acetate (Gefarnate) is an anti-ulcer *** was reported that geraniol might participate in lipid metabolism through a variety of *** aim of this study was to assess the lipid-lowering effects of gefarnate in statin-treated CAD patients with residual *** In this prospective,open-label,randomized,controlled trial,69 statin-treated CAD patients with residual hypertriglyceridemia were randomly assigned to gefarnate group and control group,received gefarnate (100 mg/3 times a day) combined with statin and statin alone,*** baseline and after one-month treatment,the levels of plasma triglyceride,high-density lipoprotein cholesterol (HDL-C),low-density lipoprotein cholesterol (LDL-C) and total cholesterol were *** After one-month gefarnate treatment,triglyceride level was significantly lowered from 2.64 mmol/L to 2.12 mmol/L(P=0.0018),LDL-C level lowered from 2.7 mmol/L to 2.37 mmol/L (P=0.0004),HDL-C level increased from 0.97 mmol/L to 1.17mmol/L (P=0.0228).Based on statin therapy,gefarnate could significantly reduce the plasma triglyceride level (P=0.0148) and increase the plasma HDL-C level (P=0.0307).Although the LDL-C and total cholesterol levels tended to decrease,there was no statistically significant *** The addition of gefarnate to statin reduced triglyceride level and increased HDL-C level to a significant extent compared to statin alone in CAD patients with residual *** suggested that gefarnate might provide the dual benefits of preventing gastrointestinal injury and lipid lowering in CAD patients.

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Lipid-lowering effects of gefarnate in statin-treated patients with residual hypertriglyceridemia: a randomized controlled study

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Journal of geriatric cardiology : JGC 2024年第8期21卷 791-798页

作者： Jing Shi Ming-Lu Xu Mei-Jiao He Wan-Lan Bo Hai-Yu Zhang Dang-Hui Sun Ding-Yu Wang Xiao-Yu Wang Qun Shao Yu-Jiao Pan Yu Zhang Chen-Guang Dai Jing-Ying Wang Lin-Wei Zhang Guang-Zhong Liu Yue Li Department of Cardiology the First Affiliated Hospital Harbin Medical University Harbin China. Department of Gastroenterology the Fourth Affiliated Hospital Harbin Medical University Harbin China. Department of Cardiology Harbin Medical University Cancer Hospital Harbin China. Department of Cardiology Shenzhen People's Hospital Shenzhen China. national key laboratory of frigid zone cardiovascular diseases Harbin Medical University Harbin China. NHC key laboratory of Cell Transplantation Key Laboratory of Cardiovascular Disease Acousto-Optic Electromagnetic Diagnosis and Treatment in Heilongjiang Province Heilongjiang Province Clinical Medical Research Center for Hypertension the First Affiliated Hospital Harbin Medical University Harbin China. Institute of Metabolic Disease Heilongjiang Academy of Medical Science Harbin China.

BACKGROUND:The prevention of coronary artery disease (CAD) faces dual challenges: the aspirin-induced gastrointestinal injury, and the residual cardiovascular risk after statin treatment. Geraniol acetate (Gefarnate) is an anti-ulcer drug. It was reported that geraniol might participate in lipid metabolism through a variety of pathways. The aim of this study was to assess the lipid-lowering effects of gefarnate in statin-treated CAD patients with residual hypertriglyceridemia.METHODS:In this prospective, open-label, randomized, controlled trial, 69 statin-treated CAD patients with residual hypertriglyceridemia were randomly assigned to gefarnate group and control group, received gefarnate (100 mg/3 times a day) combined with statin and statin alone, respectively. At baseline and after one-month treatment, the levels of plasma triglyceride, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and total cholesterol were tested.RESULTS:After one-month gefarnate treatment, triglyceride level was significantly lowered from 2.64 mmol/L to 2.12 mmol/L ( = 0.0018), LDL-C level lowered from 2.7 mmol/L to 2.37 mmol/L ( = 0.0004), HDL-C level increased from 0.97 mmol/L to 1.17 mmol/L ( = 0.0228). Based on statin therapy, gefarnate could significantly reduce the plasma triglyceride level ( = 0.0148) and increase the plasma HDL-C level ( = 0.0307). Although the LDL-C and total cholesterol levels tended to decrease, there was no statistically significant difference.CONCLUSIONS:The addition of gefarnate to statin reduced triglyceride level and increased HDL-C level to a significant extent compared to statin alone in CAD patients with residual hypertriglyceridemia. This suggested that gefarnate might provide the dual benefits of preventing gastrointestinal injury and lipid lowering in CAD patients.

关键词： nat alone Lipid

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lncRNA Gm20257 alleviates pathological cardiac hypertrophy by modulating the PGC-1α-mitochondrial complex IV axis

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FRONTIERS OF MEDICINE 2024年第4期18卷 664-677页

作者： Yu, Tong Gao, Qiang Zhang, Guofang Li, Tianyu Liu, Xiaoshan Li, Chao Zheng, Lan Sun, Xiang Wu, Jianbo Cao, Huiying Bi, Fangfang Wang, Ruifeng Liang, Haihai Li, Xuelian Zhou, Yuhong Lv, Lifang Shan, Hongli Shanghai Univ Engn Sci Inst Frontier Med Technol Shanghai Frontiers Sci Res Ctr Druggabil Cardiovas Shanghai 201620 Peoples R China Harbin Med Univ Sch Basic Med Dept Physiol Harbin 150081 Peoples R China Harbin Med Univ Ctr Funct Expt Teaching Sch Basic Med Harbin 150081 Peoples R China Harbin Med Univ Coll Pharm Dept Pharmacol State Key Lab Frigid Zone Cardiovasc DisState Pro Harbin 150081 Peoples R China

Pathological cardiac hypertrophy, a major contributor to heart failure, is closely linked to mitochondrial function. The roles of long noncoding RNAs (lncRNAs), which regulate mitochondrial function, remain largely unexplored in this context. Herein, a previously unknown lncRNA, Gm20257, was identified. It markedly increased under hypertrophic stress in vivo and in vitro. The suppression of Gm20257 by using small interfering RNAs significantly induced cardiomyocyte hypertrophy. Conversely, the overexpression of Gm20257 through plasmid transfection or adeno-associated viral vector-9 mitigated angiotensin II-induced hypertrophic phenotypes in neonatal mouse ventricular cells or alleviated cardiac hypertrophy in a mouse TAC model respectively, thus restoring cardiac function. Importantly, Gm20257 restored mitochondrial complex IV level and enhanced mitochondrial function. Bioinformatics prediction showed that Gm20257 had a high binding score with peroxisome proliferator-activated receptor coactivator-1 (PGC-1 alpha), which could increase mitochondrial complex IV. Subsequently, Western blot analysis results revealed that Gm20257 substantially affected the expression of PGC-1 alpha. Further analyses through RNA immunoprecipitation and immunoblotting following RNA pull-down indicated that PGC-1 alpha was a direct downstream target of Gm20257. This interaction was demonstrated to rescue the reduction of mitochondrial complex IV induced by hypertrophic stress and promote the generation of mitochondrial ATP. These findings suggest that Gm20257 improves mitochondrial function through the PGC-1 alpha-mitochondrial complex IV axis, offering a novel approach for attenuating pathological cardiac hypertrophy.

关键词： lncRNA Gm20257 cardiac hypertrophy PGC-1 alpha mitochondrial complex IV ATP LONG NONCODING RNA HEART-FAILURE CARDIOMYOPATHY REGULATOR

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Long non-coding RNA-AK138945 regulates myocardial ischemia-reperfusion injury via the miR-1-GRP94 signaling pathway

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frigid zone Medicine 2024年第1期4卷 31-40页

作者： Yanying Wang Jian Huang Han Sun Jie Liu Yingchun Shao Manyu Gong Xuewen Yang Dongping Liu Zhuo Wang Haodong Li Yanwei Zhang Xiyang Zhang Zhiyuan Du Xiaoping Leng Lei Jiao Ying Zhang State key laboratory of frigid zone cardiovascular diseases and Pharmacology Department of Pharmacy college of Harbin Medical UniversityHarbin 150081China The Fourth Department of Medical Oncology Harbin Medical University Cancer HospitalHarbin 150040China Department of Ultrasound Imaging the Second Affiliated Hospital of Harbin Medical UniversityHarbin 150086China Cancer Institute The Affiliated Hospital of Qingdao UniversityQingdao UniversityQingdao Cancer InstituteQingdao 266071China College of Bioinformatics Science and Technology Harbin Medical UniversityHarbin 150081China

Objective:Myocardial ischemia-reperfusion injury(MIRI)is one of the leading causes of death from cardiovascular disease in humans,especially in individuals exposed to cold *** non-coding RNAs(lncRNAs)regulate MIRI through multiple *** study explored the regulatory effect of lncRNA-AK138945 on myocardial ischemia-reperfusion injury and its ***:In vivo,8-to 12-weeks-old C57BL/6 male mice underwent ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion for 48 *** vitro,the primary cultured neonatal mouse ventricular cardiomyocytes(NMVCs)were treated with 100μmol/L hydrogen peroxide(H_(2)O_(2)).The knockdown of lncRNA-AK138945 was evaluated to detect cardiomyocyte apoptosis,and a glucose-regulated,endoplasmic reticulum stress-related protein 94(GRP94)inhibitor was used to detect myocardial ***:We found that the expression level of lncRNA-AK138945 was reduced in MIRI mouse heart tissue and H2O2-treated ***,the proportion of apoptosis in cardiomyocytes increased after lncRNA-AK138945 was *** expression level of Bcl2 protein was decreased,and the expression level of Bad,Caspase 9 and Caspase 3 protein was *** further study found that miR-1a-3p is a direct target of lncRNA-AK138945,after lncRNA-AK138945 was silenced in cardiomyocytes,the expression level of miR-1a-3p was increased while the expression level of its downstream protein GRP94 was ***,treatment with a GRP94 inhibitor(PU-WS13)intensified H2O2-induced cardiomyocyte *** overexpression of FOXO3,the expression levels of lncRNA-AK138945 and GRP94 were increased,while the expression levels of miR-1a-3p were ***:LncRNA-AK138945 inhibits GRP94 expression by regulating miR-1a-3p,leading to cardiomyocyte *** transcription factor Forkhead Box Protein O3(FOXO3)participates in cardiomyocyte apoptosis induced by endoplasmic reticulum s

关键词： myocardial ischemia reperfusion lncRNA apoptosis microRNAGRP94

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