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MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction

Animal Models and experimental Medicine 2024年第4期7卷 408-418页

作者： Guofeng Bai Jinghao Yang Weili Liao Xiaofeng Zhou Yingting He Nian Li Liuhong Zhang Yifei Wang Xiaoli Dong Hao Zhang Jinchun Pan Liangxue Lai Xiaolong Yuan Xilong Wang Guangdong Provincial Key laboratory of laboratory Animals Guangdong Laboratory Animals Monitoring InstituteGuangzhouChina Guangdong laboratory of Lingnan Modern Agriculture National Engineering Research Center for Breeding Swine IndustryState Key Laboratory of Swine and Poultry Breeding IndustryGuangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular BreedingCollege of Animal ScienceSouth China Agricultural UniversityGuangzhouGuangdongChina Huidong County Animal Quarantine and Inspection Institute HuizhouGuangdongChina Department of cardiology Hainan General HospitalHainan Affiliated Hospital of Hainan Medical UniversityHainan Clinical Medicine Research InstitutionHaikouPeople's Republic of China Key laboratory of Regenerative Biology Guangzhou Institutes of Biomedicine and HealthChinese Academy of SciencesGuangzhouGuangdongChina

Background:Myocardial infarction(MI)is an acute condition in which the heart mus-cle dies due to the lack of blood *** research has suggested that au-tophagy and angiogenesis play vital roles in the prevention of heart failure after MI,and miR-106a is considered to be an important regulatory factor in *** the specific mechanism remains *** this study,using cultured venous endothelial cells and a rat model of MI,we aimed to identify the potential target genes of miR-106a and discover the mechanisms of inhibiting autophagy and ***:We first explored the biological functions of miR-106a on autophagy and angiogenesis on endothelial *** we identified ATG7,which was the down-stream target gene of *** expression of miR-106a and ATG7 was investi-gated in the rat model of ***:We found that miR-106a inhibits the proliferation,cell cycle,autophagy and angiogenesis,but promoted the apoptosis of vein endothelial ***,ATG7 was identified as the target of miR-106a,and ATG7 rescued the inhibition of autophagy and angiogenesis by *** expression of miR-106a in the rat model of MI was decreased but the expression of ATG7 was increased in the infarction ***:Our results indicate that miR-106a may inhibit autophagy and angiogenesis by targeting *** mechanism may be a potential therapeutic treatment for MI.

关键词： angiogenesis ATG7 autophagy miR-106a miRNAs myocardial infarction

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Multi-omics Approach Reveals Influenza-A Virus Target Genes Associated Genomic,Clinical and Immunological Characteristics in Cancers

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Biomedical and Environmental Sciences 2024年第7期37卷 698-715页

作者： Jiaojiao Wang Yong Liao Pinglian Yang Weile Ye Yong Liu Chunxia Xiao Weixiong Liao Chunbo Chen Zhiping Liu Zunnan Huang Center of Scientific Research Department of CardiologyMaoming People’s HospitalMaoming 525000GuangdongChina Department of Pharmacy Maoming People’s HospitalMaoming 525000GuangdongChina State Key laboratory of Bioactive Molecules and Druggability Assessment Jinan UniversityGuangzhou 510632GuangdongChina Guangdong Province Key laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research College of PharmacyJinan UniversityGuangzhou 510632GuangdongChina Key laboratory of Big Data Mining and Precision Drug Design of Guangdong Medical University Key Laboratory of Computer-Aided Drug Design of Dongguan CityKey Laboratory for Research and Development of Natural Drugs of Guangdong ProvinceSchool of PharmacyGuangdong Medical UniversityDongguan 523808GuangdongChina Department of Critical Care Medicine Maoming People’s HospitalMaoming 525000GuangdongChina

Objective To examine the precise function of influenza A virus target genes(IATGs)in *** Using multi-omics data from the TCGA and TCPA datasets,33 tumor types were evaluated for *** expression in cancer cells was analyzed using transcriptome *** number variation(CNV)was assessed using GISTICS ***’s analysis was used to correlate mRNA expression with methylation *** was used for the enrichment ***’s correlation analysis was used to examine the association between IATG mRNA expression and *** ImmuCellAI algorithm was used to calculate the infiltration scores of 24 immune cell *** In 13 solid tumors,IATG mRNA levels were atypically *** for UCS,UVM,KICH,PCPG,THCA,CHOL,LAMI,and MESO,most cancers contained somatic IATG *** main types of CNVs in IATGs are heterozygous amplifications and *** most tumors,IATG mRNA expression is adversely associated with ***-PCR demonstrated that EGFR,ANXA5,CACNA1C,CD209,UVRAG were upregulated and CLEC4M was downregulated in KIRC cell lines,consistent with the TCGA and GTEx *** Genomic changes and clinical characteristics of IATGs were identified,which may offer fresh perspectives linking the influenza A virus to cancer.

关键词： Genomic changes Immune microenvironment Prognosis Drug resistance experimental validation

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Post-infarct cardiac injury, protection and repair:roles of non-cardiomyocyte multicellular and acellular components

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Science China(Life Sciences) 2018年第3期61卷 266-276页

作者： Xiaojun Du experimental cardiology laboratory Baker Heart and Diabetes Institute

Following myocardial infarction(MI), cardiomyocytes and infarct size are the focus of our attention when evaluating the extent of cardiac injury, efficacy of therapies or success in repairing the damaged heart by stem cell therapy. Numerous interventions have been shown by pre-clinical studies to be effective in limiting infarct size, and yet clinical trials designed accordingly have yielded disappointing outcomes. The ultimate goal of cardiac protection is to limit the adverse cardiac remodeling. Accumulating studies have revealed that post-infarct remodeling can be attenuated without infarct size limitation. To reconcile this, one needs to appreciate the significance of various cellular and acellular myocardial components that, like cardiomyocytes, undergo significant damage and dysfunction, which impact the ultimate cardiac injury and remodelling. Microvascular injury following ischemia-reperfusion may influence infarct size and promote inflammation. Myocardial injury evokes innate immunity with massive inflammatory infiltration that, although essential for the healing process, exacerbates myocardial injury and damage to extracellular matrix leading to dilative remodeling. It is also important to consider the multiple non-cardiomyocyte components in evaluating therapeutic efficacy. Current research indicates the pivotal role of these components in achieving cardiac regeneration by cell therapy. This review summarizes findings in this field, highlights a broad consideration of therapeutic targets,and recommends cardiac remodeling as the ultimate target.

关键词： myocardial infarction ventricular remodelling infarct size inflammation extracellular matrix microvascular damage autonomic nerves

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The incidence rate and histological characteristics of intimal hyperplasia in elastase-induced experimental abdominal aortic aneurysms in mice

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Animal Models and experimental Medicine 2024年第3期7卷 388-395页

作者： Meng Li Panpan Wei Kexin Li Haole Liu Naqash Alam Haiwen Hou Jie Deng Baohui Xu Enqi Liu Sihai Zhao Yankui Li laboratory Animal Center Xi'an Jiaotong UniversityXi'anChina Department of Vascular Surgery The Second Hospital of Tianjin Medical UniversityTianjinChina Department of cardiology The Second Affiliated Hospital of Xi'an Jiaotong UniversityXi'anChina Department of Vascular Surgery Stanford University School of MedicineStanfordCaliforniaUSA

Intimal hyperplasia(IH)is a negative vascular remodeling after arterial *** occasionally occurs in elastase-induced abdominal aortic aneurysm(AAA)mouse *** study aims to clarify the incidence and histological characteristics of IH in aneurysmal mice.A retrospective study was conducted by including 42 male elastaseinduced mouse AAA *** IH incidence,aortic diameters with or without IH,and hyperplasia lesional features of mice were *** 42 elastase-induced AAA mouse models,10 mice developed mild IH(24%)and severe IH was found in only 2 mice(5%).The outer diameters of the AAA segments in mice with and without IH did not show significant *** mild and severe IH lesions show strong smooth muscle cell positive staining,but endothelial cells were occasionally observed in severe IH *** was obvious macrophage infiltration in the IH lesions of the AAA mouse models,especially in mice with severe ***,only a lower numbers of T cells and B cells were found in the IH *** cell-secreted matrix metalloproteinases(MMP)2 was highly expressed in all IH lesions,but MMP9 was only overexpressed in severe *** conclusion,this study is the first to demonstrate the occurrence of aneurysmal IH and its histological characteristics in an elastaseinduced mouse AAA *** will help researchers better understand this model,and optimize it for use in AAA-related research.

关键词： abdominal aortic aneurysms animal model histology intimal hyperplasia

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A novel mouse model of calcific aortic valve stenosis

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Animal Models and experimental Medicine 2024年第4期7卷 523-532页

作者： Ningjing Qian Yaping Wang Wangxing Hu Naifang Cao Yi Qian Jinyong Chen Juan Fang Dilin Xu Haochang Hu Shuangshuang Yang Dao Zhou Hanyi Dai Dongdong Wei Jian'an Wang Xianbao Liu Department of cardiology The Second Affiliated HospitalZhejiang University School of MedicineHangzhouChina State Key laboratory of Transvascular Implantation Devices China Cardiovascular Key laboratory of Zhejiang Province HangzhouChina Department of Cardiovascular Surgery The Second Affiliated HospitalZhejiang University School of MedicineHangzhouChina Department of Endocrinology The Second Affiliated HospitalZhejiang University School of MedicineHangzhouChina Binjiang Institute of Zhejiang University HangzhouChina

Background:Calcific aortic valve stenosis(CAVS)is one of the most challenging heart diseases in clinical with rapidly increasing ***,study of the mecha-nism and treatment of CAVS is hampered by the lack of suitable,robust and efficient models that develop hemodynamically significant stenosis and typical calcium ***,we aim to establish a mouse model to mimic the development and features of ***:The model was established via aortic valve wire injury(AVWI)combined with vitamin D subcutaneous injected in wild type C57/BL6 *** transthoracic echocardiography was applied to evaluate aortic jet peak velocity and mean *** specimens were collected and examined in respect of valve thickening,calcium deposition,collagen accumulation,osteogenic differentiation and ***:Serial transthoracic echocardiography revealed that aortic jet peak velocity and mean gradient increased from 7 days post model establishment in a time depend-ent manner and tended to be stable at 28 *** with the sham group,sim-ple AVWI or the vitamin D group,the hybrid model group showed typical pathological features of CAVS,including hemodynamic alterations,increased aortic valve thicken-ing,calcium deposition,collagen accumulation at 28 *** addition,osteogenic dif-ferentiation,fibrosis and inflammation,which play critical roles in the development of CAVS,were observed in the hybrid ***:We established a novel mouse model of CAVS that could be induced efficiently,robustly and economically,and without genetic *** provides a fast track to explore the underlying mechanisms of CAVS and to identify more effec-tive pharmacological targets.

关键词： animal model calcific aortic valve stenosis valve calcification

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DEAD-box helicase 17(DDX17)protects cardiac function by promoting mitochondrial homeostasis in heart failure

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Signal Transduction and Targeted Therapy 2024年第6期9卷 2774-2790页

作者： Mingjing Yan Junpeng Gao Ming Lan Que Wang Yuan Cao Yuxuan Zheng Yao Yang Wenlin Li Xiaoxue Yu Xiuqing Huang Lin Dou Bing Liu Junmeng Liu Hongqiang Cheng Kunfu Ouyang Kun Xu Shenghui Sun Jin Liu Weiqing Tang Xiyue Zhang Yong Man Liang Sun Jianping Cai Qing He Fuchou Tang Jian Li Tao Shen The Key laboratory of Geriatrics Beijing Institute of GeriatricsInstitute of Geriatric MedicineChinese Academy of Medical SciencesBeijing Hospital/National Center of Gerontology of National Health CommissionBeijing 100730China Peking University Fifth School of Clinical Medicine Beijing 100730China Department of laboratory Medicine Huashan HospitalShanghai Medical CollegeFudan UniversityShanghai 200040China Biomedical Pioneering Innovation Center School of Life SciencesPeking UniversityBeijing 100871China Emergency Center Zhongnan Hospital of Wuhan UniversityWuhan 430071China Department of cardiology Beijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100730China Graduate School of Peking Union Medical College Beijing 100730China Department of Health Care Beijing HospitalNational Center of GerontologyInstitute of Geriatric MedicineChinese Academy of Medical SciencesBeijing 100730China Peking-Tsinghua Center for Life Sciences Academy for Advanced Interdisciplinary StudiesPeking UniversityBeijing 100871China Department of Pathology and Pathophysiology and Department of cardiology at Sir Run Run Shaw Hospital Zhejiang University School of MedicineHangzhou 310058China Department of Cardiovascular Surgery Peking University Shenzhen HospitalShenzhen 518036China experimental Technology Center for Life Sciences at Beijing Normal University Beijing 100875China

DEAD-box helicase 17(DDX17)is a typical member of the DEAD-box family with transcriptional cofactor *** DDX17 is abundantly expressed in the myocardium,its role in heart is not fully *** generated cardiomyocyte-specific Ddx17-knockout mice(Ddx17-cKO),cardiomyocyte-specific Ddx17 transgenic mice(Ddx17-Tg),and various models of cardiomyocyte injury and heart failure(HF).DDX17 is downregulated in the myocardium of mouse models of heart failure and cardiomyocyte ***-specific knockout of Ddx17 promotes autophagic flux blockage and cardiomyocyte apoptosis,leading to progressive cardiac dysfunction,maladaptive remodeling and progression to heart *** of DDX17 expression in cardiomyocytes protects cardiac function under pathological *** studies showed that DDX17 can bind to the transcriptional repressor B-cell lymphoma 6(BCL6)and inhibit the expression of dynamin-related protein 1(DRP1).When DDX17 expression is reduced,transcriptional repression of BCL6 is attenuated,leading to increased DRP1 expression and mitochondrial fission,which in turn leads to impaired mitochondrial homeostasis and heart *** also investigated the correlation of DDX17 expression with cardiac function and DRP1 expression in myocardial biopsy samples from patients with heart *** findings suggest that DDX17 protects cardiac function by promoting mitochondrial homeostasis through the BCL6-DRP1 pathway in heart failure.

关键词： DDX17 homeostasis cardiac

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Potential preservative mechanisms of cardiac rehabilitation pathways on endothelial function in coronary heart disease

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Science China Life Sciences 2024年

作者： Wen-Tao Sun Jian-Yong Du Jia Wang Yi-Long Wang Er-Dan Dong Research Center for Cardiopulmonary Rehabilitation University of Health and Rehabilitation Sciences Qingdao Hospital (Qingdao Municipal Hospital)School of Health and Life SciencesUniversity of Health and Rehabilitation Sciences Department of cardiology and Institute of Vascular Medicine Peking University Third HospitalThe Institute of Cardiovascular SciencesPeking UniversityState Key Laboratory of Vascular Homeostasis and RemodelingPeking University

Cardiac rehabilitation, a comprehensive exercise-based lifestyle and medical management, is effective in decreasing morbidity and improving life quality in patients with coronary heart disease. Endothelial function, an irreplaceable indicator in coronary heart disease progression, is measured by various methods in traditional cardiac rehabilitation pathways, including medicinal treatment, aerobic training, and smoking cessation. Nevertheless, studies on the effect of some emerging cardiac rehabilitation programs on endothelial function are limited. This article briefly reviewed the endothelium-beneficial effects of different cardiac rehabilitation pathways, including exercise training, lifestyle modification and psychological intervention in patients with coronary heart disease, and related experimental models, and summarized both uncovered and potential cellular and molecular mechanisms of the beneficial roles of various cardiac rehabilitation pathways on endothelial function. In exercise training and some lifestyle interventions, the enhanced bioavailability of nitric oxide, increased circulating endothelial progenitor cells(EPCs), and decreased oxidative stress are major contributors to preventing endothelial dysfunction in coronary heart disease. Moreover, the preservation of endothelial-dependent hyperpolarizing factors and inflammatory suppression play roles. On the one hand, to develop more endothelium-protective rehabilitation methods in coronary heart disease, adequately designed and sized randomized multicenter clinical trials should be advanced using standardized cardiac rehabilitation programs and existing assessment methods. On the other hand, additional studies using suitable experimental models are warranted to elucidate the relationship between some new interventions and endothelial protection in both macro-and microvasculature.

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Sodium-glucose cotransporter-2 inhibitors protect tissues via cellular and mitochondrial pathways:experimental and clinical evidence

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World Journal of experimental Medicine 2024年第2期14卷 46-52页

作者： Raúl Lelio Sanz Sebastián García Menéndez Felipe Inserra Leon Ferder Walter Manucha Department of Pathology Facultad de Ciencias MédicasUniversidad Nacional de CuyoMendoza 5500Argentina Department of Pharmacology Instituto de Medicina y Biología Experimental de CuyoCentro Científico TecnológicoMendoza 5500Argentina Department of Nephrology Universidad de MaimónidesCiudad Autónoma de Buenos Aires C1405Argentina Department of cardiology Universidad de MaimónidesCiudad Autónoma de Buenos Aires C1405Argentina

Mitochondrial dysfunction is a key driver of cardiovascular disease(CVD)in metabolic syndrome and *** dysfunction promotes the production of reactive oxygen species(ROS),which cause oxidative stress and *** II,the main mediator of the renin-angiotensin-aldosterone system,also contributes to CVD by promoting ROS *** activity of sirtuins(SIRTs),a family of proteins that regulate cellular metabolism,also worsens oxidative *** of energy production by mitochondria is a common feature of all metabolic *** SIRT levels and 5’adenosine monophosphate-activated protein kinase signaling stimulate hypoxia-inducible factor 1 beta,which promotes ***,in turn,increases autophagy and mitophagy,processes that clear cells of debris and protect against *** cotransporter-2 inhibitors(SGLT2i),a class of drugs used to treat type 2 diabetes,have a beneficial effect on these *** clinical trials have shown that SGLT2i improves cardiac function and reduces the rate of cardiovascular and renal ***2i also increase mitochondrial efficiency,reduce oxidative stress and inflammation,and strengthen *** findings suggest that SGLT2i hold great potential for the treatment of ***,they are proposed as anti-aging drugs;however,rigorous research is needed to validate these preliminary findings.

关键词： Sodium-glucose cotransporter-2 inhibitors Cardiovascular diseases Sirtuins Oxidative stress Inflammation Mitochondrial dysfunction

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微米尺度的规则拓扑结构对细胞和组织行为的影响

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Science China Materials 2024年第7期67卷 2090-2102页

作者：王兴旺郑晗毅汪璟余红梅唐前傅国胜任科峰计剑于路 Key laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province Department of CardiologySir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310016China MOE Key laboratory of Macromolecular Synthesis and Functionalization Department of Polymer Science and EngineeringZhejiang UniversityHangzhou310058China Department of Surgery Sir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310016China Engineering Research Center for Cardiovascular Innovative Devices of Zhejiang Province Hangzhou 310016China

生物材料表面的物理性质,如拓扑结构,由于其易于加工和稳定的生物作用而受到广泛关注.虽然已有许多研究报道了材料表面拓扑结构与细胞的相互作用,但由于不同研究中使用的微结构和实验环境的多样性,生物材料表面不同微结构与细胞/组织行... 详细信息

生物材料表面的物理性质,如拓扑结构,由于其易于加工和稳定的生物作用而受到广泛关注.虽然已有许多研究报道了材料表面拓扑结构与细胞的相互作用,但由于不同研究中使用的微结构和实验环境的多样性,生物材料表面不同微结构与细胞/组织行为之间的影响关系尚未得到很好的统一评价.在本研究中,我们设计了11种图案(三角形、矩形、圆形等),这些图案包含两种类型的形貌(微坑和微柱),这样一共得到22种表面拓扑结构.我们在体外和体内对这些微结构影响细胞和组织的生物作用进行了评估.我们的研究结果表明,由连续微坑形成的凹槽微结构促进细胞迁移效果相比其他微结构更强.其中,由三角形微坑组成的凹槽在体外对细胞迁移的促进作用最强.在大鼠皮下模型中,这种三角形微坑组成的凹槽结构减少了纤维组织的包封,促进了血管的形成.

关键词： micro-scale topography cell behavior tissue response endothelial cells biomaterials

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Chinese dwarf cherry [Cerasus humilis(Bge.) Sok.] polyphenol extract promotes osteoblastic differentiation in MC3T3-E1 cells and reduce ovariectomy-induced bone loss in rats via the calcium/AMPK signaling pathway

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Food Science and Human Wellness 2024年

作者： Yushi Zhang Qingyu Cui Lixin Wang Xiaoxue Wang Shupeng Liu Rong Zeng Weidong Li School of Chinese Materia Medica， Beijing University of Chinese Medicine Qingdao Histep Health Technology Ltd. Department of cardiology， Beijing Anzhen Hospital， Capital Medical University

Chinese dwarf cherry (Cerasus humilis) is a fruit unique to China， which is considered to have osteoprotective effects. However， no systematic experimental characterization was available. In this study， the osteoprotective activity and mechanism of Chinese dwarf cherry polyphenol extract (OPE) was studied. In vitro， OPE stimulated the alkaline phosphatase activity in the early differentiation stage， increased the osteocalcin level in the middle differentiation stage， and induced the formation of more bone-mineralized nodules in the late osteogenic stage. In vivo， OPE improved cancellous bone structure and maximum load of the femur in ovariectomized (OVX) rats. The balance between bone formation and resorption was regulated. Oxidative stress levels in the peripheral blood， liver and femur were reduced. OPE alleviated the disturbance in energy metabolism， muscle development， and muscle regulation-related signaling pathways caused by OVX and activated the calcium/adenosine monophosphate-activated protein kinase signaling pathway. Therefore， OPE is a potential dietary supplement for the prevention and treatment of osteoporosis.

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