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| 1 | microRNA‐124 Regulates Cardiomyocyte Differentiation of Bone Marrow‐Derived Mesenchymal Stem Cells Via Targeting STAT3 Signaling显示文摘 | Benzhi Cai Jianping Li Jinghao Wang Xiaobin Luo Jing Ai Yanju Liu Ning Wang Haihai Liang Mingyu Zhang Nan Chen Gang Wang Shu Xing Xin Zhou Baofeng Yang Xinyue Wang Yanjie Lu | 2012 | STEM CELLS2012，，8： | 1 |
| 2 | Mechanisms of lumbrokinase in protection of cerebral ischemia显示文摘 | Hongrui Ji Lian Wang Hui Bi Lihua Sun Benzhi Cai Yuping Wang Jinlong Zhao Zhimin Du | 2008 | European Journal of Pharmacology2008，，1： | 1 |
| 3 | Mettl3 deficiency leads to the upregulation of Cav1.2 and increases arrhythmia susceptibility in mice显示文摘Methyltransferase-like 3(Mettl3)is a component of methyltransferase complex that mediates m6A modification of RNAs,and participates in multiple biological processes.However,the role of Mettl3 in cardiac electrophysiology remains unknown.This study aims to explore the ventricular arrhythmia susceptibility of Mettl3+/–mice and the underlying mechanisms.Mice were anesthetized with 2%avertin(0.1 mL/10 g body weight)for echocardiography and programmed electrical pacing.Whole-cell patch clamp technique was used to examine the electrophysiological property of cardiomyocytes.The expression of Cav1.2 was determined by qRT-PCR and western blot analysis.The m6A medication of mRNA was examined by MeRIP-Seq and MeRIP-qPCR.No differences are found in the morphology and function of the hearts between Mettl3+/–mice and wild-type(WT)controls.The QT and QTc intervals of Mettl3+/–mice are significantly longer.High-frequency electrical stimulation showed that heterozygous knockout of Mettl3 increases ventricular arrhythmia susceptibility.The whole-cell patch-clamp recordings showed that the APD is prolonged in Mettl3+/–ventricular myocytes and more EADs were observed.The density of ICa-L is substantially increased in ventricular myocytes of Mettl3+/–mice.The pore-forming subunit of L-type calcium channel Cav1.2 is upregulated in Mettl3+/–mice,while the mRNA of its coding gene CACNA1C does not change.MeRIP-Seq and MeRIP-qPCR showed that the m6A methylation of CACNA1C mRNA is decreased in cultured Mettl3-knockdown cardiomyocytes and Mettl3+/–hearts.Collectively,deficiency of Mettl3 increases ventricular arrhythmia susceptibility due to the upregulation of Cav1.2 by reducing m6A modification on CACNA1C mRNA in mice.This study highlights the role of m6A modification in the regulation of cardiac electrophysiology. | Ling Shi Xuexin Jin Zheng Li Rui Gong Yang Guo Jiudong Ma Yang Zhang Benzhi Cai Baofeng Yang Dongmei Gong Zhenwei Pan | 2022 | Acta Biochimica et Biophysica Sinica2022，54，2： | 1 |
| 4 | Large - conductance Ca^2 + - activated K^+ currents blocked and impaired by homocysteine in human and rat mesenteric artery smooth muscle ceils显示文摘 | Benzhi Cai | 2007 | Life Sciences2007，80，： | 1 |
| 5 | Electrocardiogram abnormalities and higher body mass index as clinically applicable factors for predicting poor outcome in patients with coronavirus disease 2019显示文摘Background:Patients with coronavirus disease 2019(COVID-19)have high resource utilization.Identifying the causes of severe COVID-19 is helpful for early intervention to reduce the consumption of medical resources.Methods:We included 103 patients with COVID-19 in this single-center observational study.To evaluate the incidence,predictors,and effects of COVID-19,we analyzed demographic information,laboratory results,comorbidities,and vital signs as factors for association with severe COVID-19.Results:The incidence of severe COVID-19 was 16.5%and the percent poor outcome(including mortality,entering in ICU or transferred to a superior hospital)was 6.8%.The majority of severe COVID-19 patients had abnormal electrocardiogram(ECG)(82.35%),hypertension(76.47%)and other cardiac diseases(58.82%).Multivariate logistic regression was used to determine the predictors of severe illness.Abnormal body mass index(BMI)and ECG(P<0.05)were independent predictors of severe COVID-19.ECG abnormality was associated with increased odds of poor outcome(area under the receiver operating characteristic curves[AUC],0.793;P=0.010)and severe COVID-19(AUC,0.807;P<0.0001).Overweight was also associated with increased odds of poor outcome(AUC,0.728;P=0.045)and severe illness COVID-19(AUC,0.816;P<0.0001).Conclusion:Overweight and electrophysiological disorders on admission are important predictors of prognosis of patients with COVID-19. | Zhidan Sun Yan Hou Zheng Zhang Benzhi Cai Jinliang Li | 2022 | Frigid Zone Medicine2022，2，4： | 0 |
| 6 | Blue LED promotes the chemosensitivity of human hepatoma to Sorafenib by inducing DNA damage显示文摘Background:Phototherapies based on sunlight,infrared,ultraviolet,visible,and laser-based treatments present advantages like high curative effects,small invasion,and negligible adverse reactions in cancer treatment.We aimed to explore the potential therapeutic effects of blue light emitting diode(LED)in human hepatoma cells and decipher the underlying cellular and molecular mechanisms.Methods:Wound healing and transwell assays were employed to probe the inhibition of the invasion and migration of hepatocellular carcinoma cells in the presence of blue LED.The sphere-forming test was used to evaluate the effect of LED blue light irradiation on cancer stem cell properties.Immunofluorescence and western blotting were used to detect the changes inγ-H2AX.The Cell Counting Kit-8 assay,5-ethynyl-2′-deoxyuridine staining,and colony formation assay were used to detect the combined effect of blue LED and sorafenib on cell proliferation inhibition.Results:We demonstrated that the irradiation of blue LED light in hepatoma cells could lead to cell proliferation reduction along with the increase of cell apoptosis.Simultaneously,blue LED irradiation also markedly suppressed the migration and invasion ability of human hepatoma cells.Sphere formation analysis further revealed the decreased cancer stemness of hepatoma cells upon blue LED irradiation.Mechanistically,blue LED irradiation significantly promoted the expression of the phosphorylation of the core histone protein H2AX(γ-H2AX),a sensitive molecular marker of DNA damage.In addition,we found that the combined treatment of blue LED irradiation and sorafenib increased cancer cell sensitivity to sorafenib.Conclusion:Collectively,we demonstrated that blue LED irradiation exhibited anti-tumor effects on liver cancer cells by inducing DNA damage and could enhance chemosensitivity of cancer cells,which represents a potential approach for human hepatoma treatment. | TONG WANG JINHUAN HONG JIAJIE XIE QIAN LIU JINRUI YUE XUTING HE SHIYU GE TAO LI GUOXIN LIU BENZHI CAI LINQIANG LI YE YUAN | 2023 | BIOCELL2023，47，8： | 0 |
| 7 | Regulation of cardiomyocyte fate plasticity: a key strategy for cardiac regeneration显示文摘With the high morbidity and mortality rates,cardiovascular diseases have become one of the most concerning diseases worldwide.The heart of adult mammals can hardly regenerate naturally after injury because adult cardiomyocytes have already exited the cell cycle,which subseqently triggers cardiac remodeling and heart failure.Although a series of pharmacological treatments and surgical methods have been utilized to improve heart functions,they cannot replenish the massive loss of beating cardiomyocytes after injury.Here,we summarize the latest research progress in cardiac regeneration and heart repair through altering cardiomyocyte fate plasticity,which is emerging as an effective strategy to compensate for the loss of functional cardiomyocytes and improve the impaired heart functions.First,residual cardiomyocytes in damaged hearts re-enter the cell cycle to acquire the proliferative capacity by the modifications of cell cycle-related genes or regulation of growth-related signals.Additionally,non-cardiomyocytes such as cardiac fbroblasts,were shown to be reprogrammed into cardiomyocytes and thus favor the repair of damaged hearts.Moreover,pluripotent stem cells have been shown to transform into cardiomyocytes to promote heart healing after myocardial infarction(MI).Furthermore,in vitro and in vivo studies demonstrated that environmental oxygen,energy metabolism,extracellular factors,nerves,non-coding RNAs,etc.play the key regulatory functions in cardiac regeneration.These fndings provide the theoretical basis of targeting cellular fate plasticity to induce cardiomyocyte proliferation or formation,and also provide the clues for stimulating heart repair after injury. | Rui Gong Zuke Jiang Naufal Zagidullin Tianyi Liu Benzhi Cai | 2021 | Signal Transduction and Targeted Therapy2021，6，2： | 0 |
| 8 | LncRNA ZFAS1 regulates cardiomyocyte differentiation of human embryonic stem cells显示文摘Background:Cardiomyocytes derived from human embryonic stem cells(hESCs)are regulated by complex and stringent gene networks during differentiation.Long non-coding RNAs(lncRNAs)exert critical epigenetic regulatory functions in multiple differentiation processes.However,the involvement of lncRNAs in the differentiation of hESCs into cardiomyocytes has not yet been fully elucidated.Here,we identified the key roles of ZFAS1(lncRNA zinc finger antisense 1)in the differentiation of cardiomyocytes from hESCs.Methods:A model of cardiomyocyte differentiation from stem cells was established using the monolayer differentiation method,and the number of beating hESCs-derived cardiomyocytes was calculated.Gene expression was analyzed by quantitative real-time PCR(qRTPCR).Immunofluorescence assays were performed to assess the expression of cardiac troponin T(cTnT)andα-actinin protein in cardiomyocytes.Results:qRT-PCR showed that ZFAS1 expression in the mesoderm was significantly higher than that in embryonic stem cells,cardiac progenitor cells,and cardiomyocytes.Knockdown of ZFAS1 inhibited cardiomyocyte differentiation from hESCs,which was characterized by reduced expression of the cardiac-specific markers cTnT,α-actinin,myosin heavy chain 6(MYH6),and myosin heavy chain 7(MYH7).In contrast,ZFAS1 overexpression remarkably increased the percentage of spontaneously beating cardiomyocytes.In terms of the mechanism,we found that ZFAS1 is an antisense lncRNA at the 5′end of the protein-coding gene ZNFX1.Knockdown of ZFAS1 could increase the mRNA expression level of ZNFX1.Furthermore,qRT-PCR demonstrated that the silencing of ZNFX1 led to an increase in cardiac-specific markers that predicted the promotion of cardiomyocyte differentiation.Conclusion:Altogether,these data suggest that lncRNA-ZFAS1 is required for cardiac differentiation by functionally inhibiting the expression of ZNFX1,which may provide a reference for the treatment of heart disease to a certain extent. | YANG CAO YINING LIU YANG YU XIAOFEI GUO XIUXIU WANG WENYA MA HANJING LI ZHONGYU REN XINLU GAO SIJIA LI HAOYU JI HONGYANG CHEN HONG YAN YANAN TIAN XIN WANG BENZHI CAI | 2023 | BIOCELL2023，47，6： | 0 |
| 9 | Cyclin L1 controls cardiomyocyte proliferation and heart repair after injury显示文摘Dear Editor,Myocardial infarction(MI)is characterized by the loss of functional cardiomyocyte(CM)in the heart,resulting in cardiac systolic dysfunction and heart failure.1,2 Increasing evidence suggested that in the heart of neonatal mice after apical resection(AR),the CM can proliferate and regenerate myocardium to repair the heart.While in the heart of adult mice after MI,the CM loses the ability to re-enter the cell cycle but undergoes hypertrophic growth. | Rui Gong Xinlu Gao Yu Liu Yifu Shen Zuke Jiang Xiuxiu Wang Naufal Zagidullin Wenya Ma Ning Wang Benzhi Cai | 2023 | Signal Transduction and Targeted Therapy2023，8，7： | 0 |
| 10 | CPAL, as a New Mediator of Cardiomyocyte Metabolic Alterations and Pyroptosis, Regulates Myocardial Infarction Injury in Mice显示文摘Myocardial infarction (MI), the most serious of the ischemic heart diseases, is accompanied by myocardial metabolic disorders and the loss of cardiomyocytes. Increasing evidence has shown that long noncoding RNAs (lncRNAs) are involved in various pathological conditions such as cancer and cardiovascular diseases (CVDs), and are emerging as a novel biomarker for these disorders. This study aims to investigate the regulatory role and mechanisms of lncRNAs in myocardial remodeling in the setting of MI. We find that post-infarcted hearts exhibit a reduction of adenosine triphosphate (ATP) and an alteration of the glucose and lipid metabolism genes cluster of differentiation 36 (CD36), hexokinase 1 (HK1), and clucose transporter 4 (GLUT4), accompanied by cardiomyocyte pyroptosis. We then identify a previously unknown conserved lncRNA, AK009126 (cardiomyocyte pyroptosis-associated lncRNA, CPAL), which is remarkably upregulated in the myocardial border zone of MI mice. Importantly, the adeno-associated virus 9 (AAV9)-mediated silencing of endogenous CPAL by its short hairpin RNA (shRNA) partially abrogates myocardial metabolic alterations and cardiomyocyte pyroptosis during MI in mice. Mechanistically, CPAL is shown to bind directly to nuclear factor kappa B (NFκB) and to act as an activator of NFκB to induce NFκB phosphorylation in cardiomyocytes. We also find that CPAL upregulates caspase-1 expression at the transcriptional level and consequently promotes the release of interleukin (IL)-18 and IL-1β from cardiomyocytes. Collectively, our findings reveal the conserved lncRNA CPAL as a new regulator of cardiac metabolic abnormalities and cardiomyocyte pyroptosis in the setting of MI and suggest CPAL as a new therapeutic target to protect cardiomyocytes against ischemic injury in infarcted hearts. | Jiamin Li Hongru Xue Ning Xu Liling Gong Ming Li Sijia Li Di Huang Qingwei Zhang Pengyu Li Qingsui Li Hang Yu Yining Liu Yadong Xue Haixin Chen Jiali Liu Wanyu Zhang Mingbin Liu Siyu Chang Xianzhi Lang Xingmiao Zhao Weijie Du Benzhi Cai Ning Wang Baofeng Yang | 2023 | Engineering2023，，1： | 0 |
| 11 | Altered expression profile of long non-coding RNAs during heart aging in mice显示文摘Objective:Long noncoding RNAs(lncRNAs)play an important role in regulating the occurrence and development of cardiovascular diseases.However,the role of lncRNAs in heart aging remains poorly understood.The objective of this study was to identify differentially expressed lncRNAs in the heart of aging mice and elucidate the relevant regulatory pathways of cardiac aging.Materials and methods:Echocardiography was used to detect the cardiac function of 18-months(aged)and 3-months(young)old C57BL/6 mice.Microarray analysis was performed to unravel the expression profiles of lncRNAs and mRNAs,and qRT-PCR to verify the highly dysregulated lncRNAs.Results:Our results demonstrated that the heart function in aged mice was impaired relative to young ones.Microarray results showed that 155 lncRNAs were upregulated and 37 were downregulated,and 170 mRNAs were significantly upregulated and 44 were remarkably downregulated in aging hearts.Gene ontology analysis indicated that differentially expressed genes are mainly related to immune function,cell proliferation,copper ion response,and cellular cation homeostasis.KEGG pathway analysis showed that the differentially expressed mRNAs are related to cytokine-cytokine receptor interaction,inflammatory mediator regulation of TRP channels,and the NF-kappa B signaling pathway.Conclusion:These results imply that the differentially expressed lncRNAs may regulate the development of heart aging.This study provides a new perspective on the potential effects and mechanisms of lncRNAs in heart aging. | Xiuxiu Wang Bingjie Hua Meixi Yu Shenzhen Liu Wenya Ma Fengzhi Ding Qi Huang Lai Zhang Chongwei Bi Ye Yuan Mengyu Jin Tianyi Liu Ying Yu Benzhi Cai Baofeng Yang | 2022 | Frigid Zone Medicine2022，2，2： | 0 |
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