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Analysis of the combined effect of rs699 and rs5051 on angiotensinogen expression and hypertension

Chronic Diseases and Translational medicine 2024年第2期10卷 102-117页

作者： Nicholas R.Powell Tyler Shugg Jacob Leighty Matthew Martin Rolf P.Kreutz Michael T.Eadon Dongbing Lai Tao Lu Todd C.Skaar Division of Clinical Pharmacology Department of MedicineSchool of MedicineIndiana UniversityIndianapolisIndianaUSA Department of Pharmacology and Toxicology School of MedicineIndiana UniversityIndianapolisIndianaUSA Department of cardiology School of MedicineKrannert Institute of CardiologyIndiana UniversityIndianapolisIndianaUSA Division of Nephrology Department of MedicineSchool of MedicineIndiana UniversityIndianapolisIndianaUSA Department of Medical and Molecular Genetics School of MedicineIndiana UniversityIndianapolisIndianaUSA

Background Hypertension(HTN)involves genetic variability in the renin-angiotensin system and influences antihypertensive *** previously reported that angiotensinogen(AGT)messenger RNA(mRNA)is endogenously bound by miR-122-5p and rs699 A>G decreases reporter mRNA in the microRNA functional-assay *** AGT promoter variant rs5051 C>T is in linkage disequilibrium(LD)with rs699 A>G and increases AGT *** independent effect of these variants is understudied due to their LD therefore we aimed to test the hypothesis that increased AGT by rs5051 C>T counterbalances AGT decreased by rs699 A>G,and when these variants occur independently,it translates to HTN-related *** We used in silico,in vitro,in vivo,and retrospective models to test this *** In silico,rs699 A>G is predicted to increase miR-122-5p binding affinity by 3%.Mir-eCLIP results show rs699 is 40–45 nucleotides from the strongest microRNA-binding site in the AGT ***,rs699 A>G increases AGT mRNA in an AGT-plasmid-cDNA HepG2 expression ***-Tissue Expression(GTEx)and UK Biobank analyses demonstrate liver AGT expression and HTN phenotypes are not different when rs699 A>G occurs independently from rs5051 C>***,GTEx and the in vitro experiments suggest rs699 A>G confers cell-type-specific effects on AGT mRNA abundance,and suggest paracrine renal renin-angiotensin-system perturbations could mediate the rs699 A>G associations with *** We found that rs5051 C>T and rs699 A>G significantly associate with systolic blood pressure in Black participants in the UK Biobank,demonstrating a fourfold larger effect than in White *** studies are warranted to determine if altered antihypertensive response in Black individuals might be due to rs5051 C>T or rs699 A>*** like this will help clinicians move beyond the use of race as a surrogate for genotype.

关键词： angiotensinogen genetic and genomic medicine hypertension rs699

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Pathologically successful conversion hepatectomy for advanced giant hepatocellular carcinoma after multidisciplinary therapy:A case report and review of literature

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World Journal of Gastrointestinal Oncology 2024年第4期16卷 1647-1659页

作者： Ju-Hang Chu Lu-Yao Huang Ya-Ru Wang Jun Li Shi-Long Han Hao Xi Wen-Xue Gao Ying-Yu Cui Ming-Ping Qian Department of General Surgery Shanghai Tenth People's HospitalSchool of MedicineTongji UniversityShanghai 200072China Department of Interventional and vascular Surgery Shanghai Tenth People's HospitalSchool of MedicineTongji UniversityShanghai 200072China Department of Pathology Shanghai Tenth People's HospitalSchool of MedicineTongji UniversityShanghai 200072China Clinical Research Management Office Shanghai Tenth People’s HospitalShanghai 200072China Department of Cell biology Institute of Medical GeneticsState Key Laboratory of CardiologyTongji University School of MedicineShanghai 200331China

BACKGROUND Hepatocellular carcinoma(HCC)is one of the leading causes of death due to its complexity,heterogeneity,rapid metastasis and easy recurrence after surgical *** demonstrated that combination therapy with transcatheter arterial chemoembolization(TACE),hepatic arterial infusion chemotherapy(HAIC),Epclusa,Lenvatinib and Sintilimab is useful for patients with advanced *** SUMMARY A 69-year-old man who was infected with hepatitis C virus(HCV)30 years previously was admitted to the hospital with abdominal *** computed tomography(CT)revealed a low-density mass in the right lobe of the liver,with a volume of 12.9 cm×9.4 cm×15 cm,and the mass exhibited a“fast-in/fast-out”pattern,with extensive filling defect areas in the right branch of the portal vein and an alpha-fetoprotein level as high as 657 ng/***,he was judged to have advanced *** treatment,the patient received three months of Epclusa,three TACE treatments,two HAIC treatments,three courses of sintilimab,and twenty-one months of *** the third month of treatment,the patient developed severe side effects and had to stop immunotherapy,and the Lenvatinib dose had to be *** pathological diagnosis indicated a complete *** patient recovered well after the operation,and no tumor recurrence was *** Multidisciplinary conversion therapy for advanced enormous HCC caused by HCV infection has a significant *** drug adjustments should be made during any treatment according to the patient's tolerance to treatment.

关键词： Hepatocellular therapy Conversion hepatectomy Interventional therapy Epclusa Lenvatinib Sintilimab Case report

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Leukocyte-Specific Morrbid Promotes Leukocyte Differentiation and Atherogenesis

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Research 2024年第2期2023卷 123-137页

作者： Di Xiang Lei Jiang Qiong Yuan Yang Yu Ruiming Liu Meiting Chen Zheng Kuai Wendy Zhang Fan Yang Tingting Wu Zhiyu He Zuhui Ke Wanzi Hong Pengcheng He Ning Tan Yeying Sun Zhen Shi Xuebiao Wei Jianfang Luo Xiaoqiu Tan Yuqing Huo Gangjian Qin Chunxiang Zhang Department of cardiology Key Laboratory of Medical ElectrophysiologyMinistry of EducationInstitute of Cardiovascular ResearchThe Affiliated Hospital of Southwest Medical UniversitySouthwest Medical UniversityLuzhouSichuan 646000China Department of Biomedical Engineering School of Medicine The University of Alabama at BirminghamBirminghamAL 35233USA Department of cardiology.Guangdong Cardiovascular institute Guangdong Provincial Key Laboratory of Coronary Heart Disease PreventionGuangdong Provincial Institute of Geriatric MedicineGuangdong General HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdong 510100China vascular biology center Medical College of GeorgiaAugusta UniversityAugustaGA 30912USA

Monocyte-to-M0/M1 macrophage differentiation with unclear molecular mechanisms is a pivotal cellular event in many cardiovascular diseases including *** non-coding RNAs(lncRNAs)are a group of protein expression regulators;however,the roles of monocyte-lncRNAs in macrophage differentiation and its related vascular diseases are still *** study aims to investigate whether the novel leukocyte-specific lncRNA Morrbid could regulate macrophage differentiation and *** identified that Morrbid was increased in monocytes and arterial walls from atherosclerotic mouse and from patients with *** cultured monocytes,Morrbid expression was markedly increased during monocyte to M0 macrophage differentiation with an additional increase during M0 macrophage-to-M1 macrophage *** differentiation stimuli-induced monocyte-macrophage differentiation and the macrophage activity were inhibited by Morrbid ***,overexpression of Morrbid alone was sufficient to elicit the monocyte-macrophage *** role of Morrbid in monocyte-macrophage differentiation was also identified in vivo in atherosclerotic mice and was verified in Morrbid knockout *** identified that PI3-kinase/Akt was involved in the up-regulation of Morrbid expression,whereas s100a10 was involved in Morrbid-mediated effect on macrophage *** provide a proof of concept of Morrbid in pathogenesis of monocyte/macrophage-related vascular disease,we applied an acute atherosclerosis model in *** results revealed that overexpression of Morrbid enhanced but monocyte/macrophage-specific Morrbid knockout inhibited the monocytes/macrophages recruitment and atherosclerotic lesion formation in *** results suggest that Morrbid is a novel biomarker and a modulator of monocyte-macrophage phenotypes,which is involved in atherogenesis.

关键词： inhibited Mor markedly

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High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p

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Science China(Life Sciences) 2024年第2期67卷 286-300页

作者： Bi-Ang Kang Hua-Ming Li Ya-Ting Chen Meng-Jie Deng Yan Li Yue-Ming Peng Jian-Jun Gao Zhi-Wei Mo Jia-Guo Zhou Zhi-Jun Ou Jing-Song Ou Division of Cardiac Surgery Cardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of vascular Diseases Guangzhou 510080China NHC key Laboratory of Assisted Circulation(Sun Yat-sen university) Guangzhou 510080China Guangdong Provincial Engineering and Technology center for Diagnosis and Treatment of vascular Diseases Guangzhou 510080China Division of vascular Surgery The First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Department of Pharmacology Cardiac and Cerebral Vascular Research CenterZhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China Division of Hypertension and vascular Diseases Department of CardiologyCardiovascular Diseases InstituteThe First Affiliated HospitalSun Yat-sen UniversityGuangzhou 510080China Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhou 510080China

We previously demonstrated that normal high-density lipoprotein(nHDL)can promote angiogenesis,whereas HDL from patients with coronary artery disease(d HDL)is dysfunctional and impairs *** plays a critical role in angiogenesis,and HDL regulates ***,it is unclear whether n HDL and d HDL regulate angiogenesis by affecting *** cells(ECs)were treated with n HDL and d HDL with or without an autophagy ***,endothelial nitric oxide synthase(e NOS)expression,miRNA expression,nitric oxide(NO)production,superoxide anion(O2^(·-))generation,EC migration,and tube formation were evaluated.n HDL suppressed the expression of miR-181a-5p,which promotes autophagy and the expression of e NOS,resulting in NO production and the inhibition of O2^(·-)generation,and ultimately increasing in EC migration and tube formation.d HDL showed opposite effects compared to n HDL and ultimately inhibited EC migration and tube *** found that autophagy-related protein 5(ATG5)was a direct target of ***5 silencing or miR-181a-5p mimic inhibited n HDL-induced autophagy,e NOS expression,NO production,EC migration,tube formation,and enhanced O2^(·-)generation,whereas overexpression of ATG5 or miR-181a-5p inhibitor reversed the above effects of d ***5 expression and angiogenesis were decreased in the ischemic lower limbs of hypercholesterolemic low-density lipoprotein receptor null(LDLr^(-/-))mice when compared to C57BL/6 ***5 overexpression improved angiogenesis in ischemic hypercholesterolemic LDLr^(-/-)*** together,nHDL was able to stimulate autophagy by suppressing miR-181a-5p,subsequently increasing e NOS expression,which generated NO and promoted *** contrast,d HDL inhibited angiogenesis,at least partially,by increasing miR-181a-5p expression,which decreased autophagy and e NOS expression,resulting in a decrease in NO production and an increase in O2^(·-)*** findings reveal a nov

关键词： high-density lipoprotein angiogenesis autophagy ATG5 miRNA endothelial nitric oxide synthase

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RIPK1 plays a crucial role in maintaining regulatory T-Cell homeostasis by inhibiting both RIPK3-and FADD-mediated cell death

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Cellular & Molecular Immunology 2024年第1期21卷 80-90页

作者： Xiaoxue Deng Lingxia Wang Yunze Zhai Qiuyue Liu Fengxue Du Yu Zhang Wenxing Zhao Tingtao Wu Yiwen Tao Jie Deng Yongbing Cao Pei Hao Jiazi Ren Yunli Shen Zuoren Yu Yuejuan Zheng Haibing Zhang Haikun Wang State Key Laboratory of cardiology Shanghai East HospitalTongji University School of MedicineShanghai200120China CAS Key Laboratory of Molecular Virology and Immunology Shanghai Institute of Immunity and InfectionChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai200031China CAS Key Laboratory of Nutrition Metabolism and Food SafetyShanghai Institute of Nutrition and HealthShanghai Institutes for Biological SciencesUniversity of Chinese Academy of SciencesChinese Academy of SciencesShanghai200031China The Research center for Traditional Chinese medicine Shanghai Institute of Infectious Diseases and BiosecurityShanghai University of Traditional Chinese MedicineShanghai201203China institute of vascular Disease Shanghai TCM-Integrated HospitalShanghai University of Traditional Chinese MedicineShanghai200433China

Regulatory T(T_(reg))cells play an essential role in maintaining immune balance across various physiological and pathological ***,the mechanisms underlying T_(reg)homeostasis remain incompletely ***,we report that RIPK1 is crucial for T_(reg) cell survival and *** generated mice with T_(reg) cell-specific ablation of Ripk1 and found that these mice developed fatal systemic autoimmunity due to a dramatic reduction in the Treg cell compartment caused by excessive cell *** conventional T cells,Treg cells with Ripk1 deficiency were only partially rescued from cell death by blocking FADD-dependent ***,simultaneous removal of both Fadd and Ripk3 completely restored the homeostasis of Ripk1-deficient Treg cells by blocking two cell death ***,our study highlights the critical role of RIPK1 in regulating Treg cell homeostasis by controlling both apoptosis and necroptosis,thereby providing novel insights into the mechanisms of Treg cell homeostasis.

关键词： Treg cell Homeostasis Apoptosis Necroptosis

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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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Smooth muscle cell-specific genetic targeting by Myh11-driven Cre(ER)knockin mice

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Science China(Life Sciences) 2024年第10期67卷 2280-2282页

作者： Enci Wang Ximeng Han Haixiao Wang Kathy O.Lui Bin Zhou Lixin Wang Department of vascular Surgery Zhongshan HospitalFudan UniversityShanghai 200032China Department of cardiology Shanghai Chest HospitalShanghai Jiao Tong University School of MedicineShanghai 200030China Pediatric Research institute The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou 325027China Department of Chemical Pathology and Li Ka Shing Institute of Health SciencesPrince of Wales HospitalThe Chinese University of Hong KongHong Kong 999077China New Cornerstone Investigator institute State Key Laboratory of Cell BiologyShanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai 200031China Department of vascular Surgery(Xiamen) Zhongshan hospitalFudan UniversityXiamen 361015China

Dear editor,Site specific recombinases have been widely used for genome engineering in cardiovascular research(Fu et al.,2024;Huang et al.,2023;Xue et al.,2022).In particular,Cre is the most broadly used recombinase for cell type-specific lineage tracing and gene manipulation in *** smooth muscle cell(SMC)-specific targeting,several SMC promoters including Myh11(smooth muscle myosin heavy chain),Acta2(smooth muscle a-2 actin),and SM22a(Tagln)have been used to drive Cre or CreER.

关键词： cardiovascular manipulation

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Increase of PCSK9 expression in diabetes promotes VEGFR2ubiquitination to inhibit endothelial function and skin wound healing

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Science China Life Sciences 2024年

作者： Jian-Jun Gao Fang-Yuan Wu Yu-Jia Liu Le Li Yi-Jun Lin Yue-Ting Kang Yue-Ming Peng Yi-Fang Liu Chen Wang Zhen-Sheng Ma Yang Cao Hong-Yu Cao Zhi-Wei Mo Yan Li Jing-Song Ou Zhi-Jun Ou Division of Cardiac Surgery Cardiovascular Diseases Institute The First Affiliated Hospital Sun Yat-sen University National-Guangdong Joint Engineering Laboratory for Diagnosis and Treatment of vascular Diseases NHC key Laboratory of Assisted Circulation and Vascular Diseases (Sun Yat-sen University) Key Laboratory of Assisted Circulation and Vascular Diseases Chinese Academy of Medical Sciences Guangdong Provincial Engineering and Technology Center for Diagnosis and Treatment of Vascular Diseases Division of Hypertension and vascular Diseases Department of Cardiology Heart Center The First Affiliated Hospital Sun Yat-sen University Division of vascular Surgery The First Affiliated Hospital Sun Yat-sen University Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of Medicine Sun Yat-sen University

Diabetic foot ulcers（DFUs） are a serious vascular disease. Currently, no effective methods are available for treating DFUs. Pro-protein convertase subtilisin/kexin type 9（PCSK9） regulates lipid levels to promote atherosclerosis. However, the role of PCSK9 in DFUs remains unclear. In this study, we found that the expression of PCSK9 in endothelial cells（ECs） increased significantly under high glucose（HG）stimulation and in diabetic plasma and vessels. Specifically, PCSK9 promotes the E3 ubiquitin-protein ligase NEDD4 binding to vascular endothelial growth factor receptor 2（VEGFR2）, which led to the ubiquitination of VEGFR2, resulting in its degradation and downregulation in ECs. Furthermore, PCSK9 suppresses the expression and activation of AKT, endothelial nitric oxide synthase（eNOS）, and ERK1/2, leading to decreased nitric oxide（NO） production and increased superoxide anion(O2·-) generation, which impairs vascular endothelial function and angiogenesis. Importantly, using evolocumab to limit the increase in PCSK9 expression blocked the HG-induced inhibition of NO production and the increase in O2·-production, as well as inhibited the phosphorylation and expression of AKT, eNOS, and ERK1/***, evolocumab improved vascular endothelial function and angiogenesis, and promoted wound healing in diabetes. Our findings suggest that targeting PCSK9 is a novel therapeutic approach for treating DFUs.

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Physical Training and Cardioprotection

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中国运动医学杂志 2003年第4期22卷 378-382页

作者： Keith L.March indiana center for vascular biology and medicine krannert institute of cardiology indiana university school of medicine

Experimental, clinical and epidemiologic studies have provided strong evidence that physical training has beneficial effects on cardiovascular health. Numerous investigations have demonstrated that exercise increases coronary blood flow and myocardial perfusion. Importantly, training also can stimulate angiogenesis and accelerate collateral vessel growth in animal models with coronary artery occlusion. Cardiac adaptation such as increased vascularity or capillary density has been evidenced after regular endurance exercises. More recently, several studies indicate that physical training induces high levels of myocardial heat shock protein and antioxidant protein expression, which may play an important role in myocardial protection against ischemia-reperfusion injury.

关键词：心脏保护体育疗法血管生成心肌缺血再灌注损伤

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Cardiovascular toxicity with CTLA-4 inhibitors in cancer patients:A meta-analysis

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Cancer Innovation 2024年第3期3卷 49-64页

作者： Huiyi Liu Lu Fu Shuyu Jin Xingdong Ye Yanlin Chen Sijia Pu Yumei Xue Department of cardiology Guangdong Cardiovascular InstituteGuangdong Provincial People's HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdongChina The Second school of Clinical medicine Southern Medical UniversityGuangzhouGuangdongChina school of medicine South China University of TechnologyGuangzhouGuangdongChina Guangdong Provincial Key Laboratory of Clinical Pharmacology Research Center of Medical SciencesGuangdong Provincial People's HospitalGuangdong Academy of Medical SciencesGuangzhouGuangdongChina

Background:With the emergence of cytotoxic T lymphocyte-associated protein-4(CTLA-4)inhibitors,the outcomes of patients with malignant tumors have improved ***,the incidence of cardiovascular adverse events has also increased,which can affect tumor *** this study,we evaluated the incidence and severity of adverse cardiovascular events caused by CTLA-4 inhibitors by analyzing reported trials that involved CTLA-4 inhibitor ***:Randomized clinical trials published in English from January 1,2013,to November 30,2022,were searched using the Cochrane Library and PubMed *** included trials examined all grade and grades 3–5 cardiac and vascular adverse *** involved comparisons of CTLA-4 inhibitors to placebo,CTLA-4 inhibitors plus chemotherapy to chemotherapy alone,CTLA-4 inhibitors combined with PD-1/PD-L1 inhibitors to PD-1/PD-L1 inhibitors alone,and CTLA-4 inhibitors plus target agent to PD-1/PD-L1 inhibitors plus target *** odds ratio(OR)and corresponding 95%confidence intervals(CIs)were calculated using the Mantel-Haenszel ***:Overall,20 trials were ***-4 inhibitors significantly increased the incidence of all-grade cardiovascular toxicity(OR=1.33,95%CI:1.00–1.75,p=0.05).The incidence of all-grade cardiovascular toxicity increased in malignant tumor patients who received single-agent CTLA-4 inhibitors(OR=1.73,95%CI:1.13–2.65,p=0.01),as well as the incidence rate of grades 3–5 cardiovascular adverse events(OR=2.00,95%CI:1.08–3.70,p=0.03).Compared with the non-CTLA-4 inhibitor group,CTLA-4 inhibitors plus chemotherapy,PD-1/PD-L1 inhibitors,or target agent did not significantly affect the incidence of cardiac and vascular *** incidence of grades 3–5 cardiac failure,hypertension,pericardial effusion,myocarditis,and atrial fibrillation were much higher among patients exposed to CTLA-4 inhibitor,but the data were not statistically ***:Our findings suggest that the

关键词： cardiovascular toxicity CTLA-4 inhibitors malignancies

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