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[PMID]: 29524604
[Au] Autor:de Oliveira da Silva B; Alberici LC; Ramos LF; Silva CM; da Silveira MB; Dechant CRP; Friedman SL; Sakane KK; Gonçalves LR; Moraes KCM
[Ad] Address:Núcleo de Pesquisa em Biologia, Universidade Federal de Ouro Preto, UFOP, Ouro Preto, MG, Brazil; Molecular Biology Laboratory, Department of Biology, Bioscience Institute, Universidade Estadual Paulista "Júlio de Mesquita Filho", UNESP, Rio Claro, SP, Brazil.
[Ti] Title:Altered global microRNA expression in hepatic stellate cells LX-2 by angiotensin-(1-7) and miRNA-1914-5p identification as regulator of pro-fibrogenic elements and lipid metabolism.
[So] Source:Int J Biochem Cell Biol;, 2018 Mar 07.
[Is] ISSN:1878-5875
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The development of new therapeutic strategies to control or reverse hepatic fibrosis requires thorough knowledge about its molecular and cellular basis. It is known that the heptapeptide angiotensin-(1-7) [ang-(1-7)] can reduce hepatic fibrosis and steatosis in vivo; therefore, it is important to uncover the mechanisms regulating its activity and cellular model of investigation. Ang-(1-7) is a peptide of the renin-angiotensin system (RAS), and here we investigated its modulatory effect on the expression pattern of microRNAs (miRNAs) in hepatic stellate cells (HSCs) LX-2, which transdifferentiate into fibrogenic and proliferative cells. We compared the miRNA profiles between quiesced, activated and ang-(1-7)-treated activated HSCs to identify miRNAs that may regulate their transdifferentiation. Thirteen miRNAs were pointed, and cellular and molecular analyses identified miRNA-1914-5p as a molecule that contributes to the effects of ang-(1-7) on lipid metabolism and on the pro-fibrotic environment control. In our cellular model, we also analyzed the regulators of fatty acid metabolism. Specifically, miRNA-1914-5p regulates the expression of malonyl-CoA decarboxylase (MLYCD) and phosphatidic acid phosphohydrolase (PAP or Lipin-1). Additionally, Lipin-1 was closely correlated with mRNA expression of peroxisome proliferator-activated receptors (PPAR)-α and -γ, which also contribute to lipid homeostasis and to the reduction of TGF-ß1 expression. These findings provide a novel link between RAS and lipid metabolism in controlling HSCs activation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 59882 MEDLINE  
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[PMID]: 29410030
[Au] Autor:Pinheiro-Júnior EL; Boldrini-França J; de Campos Araújo LMP; Santos-Filho NA; Bendhack LM; Cilli EM; Arantes EC
[Ad] Address:School of Pharmaceutical Sciences of Ribeirão Preto (FCFRP), University of São Paulo, Ribeirão Preto, SP, Brazil.
[Ti] Title:LmrBPP9: A synthetic bradykinin-potentiating peptide from Lachesis muta rhombeata venom that inhibits the angiotensin-converting enzyme activity in vitro and reduces the blood pressure of hypertensive rats.
[So] Source:Peptides;102:1-7, 2018 Feb 02.
[Is] ISSN:1873-5169
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bradykinin-potentiating peptides (BPPs) are an important group of toxins present in Lachesis muta rhombeata venom. They act directly at renin-angiotensin-aldosterone system, through the inhibition of angiotensin-converting enzyme (ACE). This action may contribute to the hypotensive shock observed during the envenoming by this species. Thus, the main goal of this study was the solid-phase synthesis of a BPP found in L. m. rhombeata venom and its in vitro and in vivo characterization in relation to ACE inhibition and hypotensive activity, respectively. The LmrBPP9 peptide was synthesized using an automated solid-phase peptide synthesizer and purified by reversed-phase fast protein liquid chromatography (FPLC). The in vitro IC50 of the synthetic peptide is 4.25 ±â€¯0.10 µM, showing a great capacity of ACE inhibition. The in vivo studies showed that LmrBPP9 induces blood pressure reduction, both in normotensive and hypertensive rats, being more pronounced in the last ones. These results agree with the in vitro results, showing that the synthetic peptide LmrBPP9 is a potential molecule to the development of a new antihypertensive drug.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 59882 MEDLINE  
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[PMID]: 29270765
[Au] Autor:Hamano T
[Ad] Address:Department of Comprehensive Kidney Disease Research (CKDR), Osaka University Graduate School of Medicine, D11, 2-2 Yamadaoka, Suita, Osaka, Japan. hamatea@kid.med.osaka-u.ac.jp.
[Ti] Title:Vitamin D and renal outcome: the fourth outcome of CKD-MBD? Oshima Award Address 2015.
[So] Source:Clin Exp Nephrol;22(2):249-256, 2018 Apr.
[Is] ISSN:1437-7799
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Bone fracture, cardiovascular events, and mortality are three outcomes of chronic kidney disease-mineral and bone disorder (CKD-MBD), and the umbrella concept originally described for dialysis patients. The reported association of serum phosphorus or fibroblast growth factor 23 (FGF23) levels with renal outcome suggests that the fourth relevant outcome of CKD-MBD in predialysis patients is renal outcome. We found that proteinuria of 2+ or greater with a dipstick test was associated with low vitamin D status due to urinary loss of 25-hydroxyvitamin D (25D). Moreover, active vitamin D or its analogues decrease proteinuria. Given our finding that maxacalcitol does not repress renin, the reduction of proteinuria by this agent is likely due to direct upregulation of the nephrin and podocin in podocytes. Moreover, this agent downregulates the mesenchymal marker desmin in podocytes and blocks transforming growth factor-beta autoinduction, leading to attenuation of renal fibrosis in a unilateral ureteral obstructive (UUO) model. These facts are reminiscent of the suppression of epithelial-mesenchymal transition (EMT) by vitamin D. EMT blockage may explain our finding that vitamin D prescription in renal transplant recipients is associated with a lower incidence of cancer. We also reported that low vitamin D status and high FGF23 levels predict a worse renal outcome. However, administration of massive doses of 25D exacerbates renal fibrosis in UUO kidneys in 1alpha-hydroxylase knockout mice. Moreover, FGF23 inhibits 1alpha-hydroxylase in proximal tubules and monocytes. Taken together, local 1,25(OH) D in the kidney tissue but not 25D seems to protect the kidney.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1007/s10157-017-1517-3

  4 / 59882 MEDLINE  
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[PMID]: 29523869
[Au] Autor:Mogi M; Kohara K; Tabara Y; Tsukuda K; Igase M; Horiuchi M
[Ad] Address:Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Tohon, Japan. mmogi@m.ehime-u.ac.jp.
[Ti] Title:Correlation between the 24-h urinary angiotensinogen or aldosterone level and muscle mass: Japan shimanami health promoting program study.
[So] Source:Hypertens Res;, 2018 Mar 09.
[Is] ISSN:1348-4214
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Our previous report indicated that sarcopenia is associated with arterial stiffness and cardiovascular death. The renin-angiotensin system (RAS) plays an important role in cardiovascular disease and its activation may be correlated with sarcopenia according to basic research. However, few clinical studies have assessed the correlation between skeletal muscle loss and RAS component concentrations in healthy subjects. The purpose of this study was to investigate the relationships between the excretion of angiotensinogen (AGT) and aldosterone (Ald) in 24-h urine samples and clinical and sarcopenic indices. A total of 344 people participated in a voluntary medical check-up program, "Anti-Aging Doc", and underwent measurement of their sarcopenia-related indices. Urine samples were collected for 24-h within 8 weeks after a medical check-up using a partition cup and a proportional sampling method. Urine AGT and Ald levels were evaluated by enzyme-linked immunosorbent assay (ELISA). After compensating for possible confounding parameters, including baPWV, the 24-h urinary excretion of AGT was independently and negatively associated with the thigh muscle cross-sectional area. On the other hand, urinary Ald excretion was not associated with sarcopenia-related indices after compensation, even though it showed a modest but significantly positive association with sarcopenic indices in single regression analysis. Urinary AGT was related to sarcopenic indices and may be involved in the pathogenesis of sarcopenia. On the other hand, urinary Ald was not related to sarcopenic indices when considering other risk factors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1038/s41440-018-0021-9

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[PMID]: 29523271
[Au] Autor:Aung M; Konoshita T; Moodley J; Gathiram P
[Ad] Address:Department of Family Medicine, School of Nursing and Public Health, University of KwaZulu-Natal, Durban, South Africa. Electronic address: myint.aung@kznhealth.gov.za.
[Ti] Title:Association of gene polymorphisms of aldosterone synthase and angiotensin converting enzyme in pre-eclamptic South African Black women.
[So] Source:Pregnancy Hypertens;11:38-43, 2018 Jan.
[Is] ISSN:2210-7797
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The exact cause of preeclampsia (PE) remains elusive. Recently, many researchers have focused on the role of genetic variations in pathogenesis of PE. The renin-angiotensin-aldosterone system is affected in the pathogenesis of PE. OBJECTIVES: To determine association of gene polymorphisms of aldosterone synthase (CYP11B2) and angiotensin converting enzyme (ACE) in PE and normotensive South African Black women. METHODS: A group of 603 South African Black pregnant women, 246 normotensive and 357 with PE, was recruited. Purified DNA was extracted from venous blood. The distribution and frequencies of gene polymorphisms of CYP11B2 (C-344T) and ACE deletion/insertion (D/I) were determined by real time polymerase chain reaction. RESULTS: As the main outcome measure, the risk of C allele for PE was 1.28 (95%CI: 0.94-1.74; p = .1) for all allele comparisons. Thus no significant association with development of PE was observed for the CYP11B2 variants. However, post analysis of the distribution of TT genotypes of CYP11B2 were higher in the HIV uninfected normotensive than in the HIV uninfected PE group (OR: 0.47, 95%CI: 0.27-0.79, p = .0027). The C alleles of late-onset PE and HIV uninfected PE were higher than all normotensive and HIV uninfected normotensive (OR: 1.47, 95%CI: 1.02-2.10, p = .03 and OR: 1.77, 95%CI: 1.13-2.81, p = .0094 respectively). The CT genotype of CYP11B2 was statistically significant between normotensive and PE in HIV uninfected groups (OR: 2.24, 95%CI: 1.28-3.98, p = .0026). There was no significant difference in frequencies of D/I for ACE gene in PE.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  6 / 59882 MEDLINE  
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[PMID]: 29522074
[Au] Autor:Maiolino G; Battistel M; Barbiero G; Bisogni V; Rossi GP
[Ad] Address:Clinica dell'Ipertensione Arteriosa, Department of Medicine - DIMED, University of Padua, Italy.
[Ti] Title:Cure With Cryoablation of Arterial Hypertension Due to a Renin-Producing Tumor.
[So] Source:Am J Hypertens;, 2018 Mar 07.
[Is] ISSN:1941-7225
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: We herein report on a 20 years old woman with stage I hypertension, who was found to carry a renin-producing tumor (RPT). METHODS: Due to her young age, the patient underwent screening measurement of plasma renin and aldosterone, abdominal computed tomography (CT) angiography, and selective renal vein renin assessment to identify secondary hypertension. RESULTS: The patient was screened for secondary causes of hypertension and was diagnosed with secondary aldosteronism. Therefore, she underwent an abdominal computed tomography (CT) angiography that was reported as unremarkable. Selective renal vein renin studies showed overproduction of renin in the right kidney and a re-evaluation of her CT allowed detection of an 8-mm mass in her right kidney, suggesting the presence of a RPT. Considering the technical difficulty of renal sparing surgery a CT-guided cryoablation was undertaken, which provided long-term cure of arterial hypertension and normalization of plasma active renin concentration. CONCLUSIONS: RPTs usually present with a clinical phenotype featuring stage III and/or malignant hypertension and are held to be exceptionally rare. This case is unique in that it presented with stage I hypertension and a mild clinical phenotype. Moreover, to our knowledge this is the first case of RPTs shown to be safely treated with CT-guided cryoablation and found to be cured at long-term.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1093/ajh/hpx213

  7 / 59882 MEDLINE  
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[PMID]: 29521603
[Au] Autor:Stodola TJ; Liu P; Liu Y; Vallejos A; Geurts AM; Greene AS; Liang M
[Ad] Address:Physiology, Medical College of Wisconsin, United States.
[Ti] Title:Genome-wide map of proximity linkage to renin proximal promoter in rat.
[So] Source:Physiol Genomics;, 2018 Mar 09.
[Is] ISSN:1531-2267
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A challenge to understanding enhancer-gene relationships is that enhancers are not always sequentially close to the gene they regulate. Physical proximity mapping through sequencing can provide an unbiased view of the chromatin close to the proximal promoter of the renin gene (Ren). Our objective was to determine genomic regions that physically interact with the renin proximal promoter, using two different genetic backgrounds, the Dahl salt sensitive and normotensive SS-13BN, which have been shown to have different regulation of plasma renin in vivo. The chromatin conformation capture method with sequencing focused at the Ren proximal promoter in rat-derived cardiac endothelial cells was used. Cells were fixed, chromatin close to the Ren promoter was captured, and fragments were sequenced. The clustering of mapped reads produced a genome-wide map of chromatin in contact with the Ren promoter. The largest number of contacts were found on chromosome 13, the chromosome with Ren, and contacts were found on all other chromosomes except chromosome X. These contacts were significantly enriched with genes positively correlated with Ren expression and with mapped quantitative trait loci (QTLs) associated with blood pressure, cardiovascular and renal phenotypes. The results were reproducible in an independent biological replicate and in endothelial cells derived from a second rat stain. The findings reported here represent the first map between a critical cardiovascular gene and physical interacting loci throughout the genome, and will provide the basis for several new directions of research.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1152/physiolgenomics.00132.2017

  8 / 59882 MEDLINE  
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[PMID]: 29521545
[Au] Autor:Vasileiadis IE; Goudis CA; Giannakopoulou PT; Liu T
[Ad] Address:a Department of Cardiology , General Hospital of Thessaloniki G. Papanikolaou , Thessaloniki , Greece.
[Ti] Title:Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: A Promising Medication for Chronic Obstructive Pulmonary Disease?
[So] Source:COPD;:1-9, 2018 Mar 09.
[Is] ISSN:1541-2563
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Chronic obstructive pulmonary disease (COPD) is a complex disorder that primarily affects the lungs and is characterized not only by local pulmonary, but also by systemic inflammation which promotes the development of extrapulmonary and cardiovascular co-morbidities. Angiotensin converting enzyme (ACE) inhibitors and ARBs (angiotensin receptor blockers) are widely used drugs in the treatment of cardiovascular diseases, with growing evidence suggesting potential benefits in COPD patients. The purpose of this review is to describe the correlation of renin-angiotensin system (RAS) with COPD pathophysiology and to present the latest data regarding the potential role of RAS blockers in COPD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1080/15412555.2018.1432034

  9 / 59882 MEDLINE  
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[PMID]: 29521315
[Au] Autor:Örsçelik Ö; Özkan B; Arslan A; Sahin EE; Sakarya O; Sürmeli OA; Balci Fidanci S; Çelik A; Çimen BY; Özcan IT
[Ad] Address:Department of Cardiology, Faculty of Medicine, Mersin University; Mersin-Turkey. ozcanorscelik@yahoo.com.
[Ti] Title:Relationship between intrarenal renin-angiotensin activity and re-hospitalization in patients with heart failure with reduced ejection fraction.
[So] Source:Anatol J Cardiol;19(3):205-212, 2018 Mar.
[Is] ISSN:2149-2271
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Heart failure (HF) is a clinical syndrome resulting from structural or functional damages. Although clinical trials have shown that the plasma renin-angiotensin system (RAS) activation decreases HF functional status and increases hospitalization for HF patients, the effect of intrarenal RAS activity is still unknown. In this study, we investigated the relationship between the New York Heart Association (NYHA) class, duration, and number of hospitalizations in the previous year and urinary angiotensinogen (UAGT) in patients with HF with reduced ejection fraction (HFrEF). METHODS: This study included 85 patients who had an ejection fraction of <40% and were receiving optimal medical treatment. Among these, 22 were excluded from the study for various reasons. Demographically and biochemically, the remaining 63 patients were compared according to the NYHA functional classes and re-hospitalization status. RESULTS: When the groups were compared in terms of N-terminal pro-B-type natriuretic peptide (NT-proBNP), UAGT, and high-sensitivity C-reactive protein (Hs-CRP), it was found that these parameters were significantly higher in patients who were hospitalized more than two times in the previous year [p<0.001; p=0.007; p<0.001, respectively]. There was a significant correlation between number of hospitalizations and NT-proBNP (r=0.507, p<0.001), Hs-CRP (r=0.511, p<0.001), hemoglobin (r=-0.419, p=0.001), serum sodium (r=-0.26, p=0.04), and systolic blood pressure (r=-0.283, p=0.02). When the independence of multiple correlations was assessed using multiple linear regression analysis, NT-proBNP, Hs-CRP, and hemoglobin levels were independent predictors of re-hospitalization, but this was not the same for UAGT. CONCLUSION: Although UAGT levels are high in patients with poor NYHA functional class and repeated hospitalizations, this marker is not valuable for predicting repeated hospitalization in patients with HFrEF.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.14744/AnatolJCardiol.2018.68726

  10 / 59882 MEDLINE  
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[PMID]: 29520629
[Au] Autor:Clasen SC; Wald JW
[Ad] Address:Cardio-oncology in the Division of Cardiology, Hospital of the University of Pennsylvania, 3400 Civic Center Boulevard, South Pavilion 11th Floor, Philadelphia, PA, 19104, USA. Suparna.clasen@uphs.upenn.edu.
[Ti] Title:Left Ventricular Dysfunction and Chemotherapeutic Agents.
[So] Source:Curr Cardiol Rep;20(4):20, 2018 Mar 08.
[Is] ISSN:1534-3170
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: We aim to summarize the effect of cancer therapy-related cardiotoxicity on the development of left ventricular (LV) dysfunction. RECENT FINDINGS: We discuss commonly used cancer therapeutics that have the potential for both acute and delayed cardiotoxicity. LV dysfunction from cancer therapies may be found by routine cardiac imaging prior to clinical manifestations of heart failure (HF) and we discuss the current multi-modality approaches for early detection of toxicity with the use of advanced echocardiographic parameters including strain techniques. Further, we discuss the role of biomarkers for detection of LV dysfunction from cancer therapies. Current approaches monitoring and treating LV dysfunction related to cancer therapy-related cardiotoxicity include addressing modifiable cardiovascular risk factors especially hypertension and early initiation of neurohormonal blockade (NHB) with disease-modifying beta-blockers and renin-angiotensin-aldosterone system (RAAS) inhibitors. Once LV dysfunction is identified, traditional ACC/AHA guideline-directed therapy is employed. Further, we highlight the use of advanced heart failure therapies including mechanical resynchronization devices, the use of durable ventricular assist devices, and cardiac transplantation as increasingly employed modalities for treatment of severe LV dysfunction and advanced heart failure in the cardio-oncology population. This review seeks to highlight the importance of early detection, treatment, and prevention of LV dysfunction from cancer therapy-related cardiotoxicity.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s11886-018-0967-x


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