Journal of the Renin-Angiotensin-Aldosterone System最新文献

{"title":"Angiotensin II, III, and IV may be important in the progression of COVID-19.","authors":"Erkan Cure, Tevfik Bulent Ilcol, Medine Cumhur Cure","doi":"10.1177/1470320320972019","DOIUrl":"https://doi.org/10.1177/1470320320972019","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Dear Editor, The long-term consequences of SARS-CoV-2 infection and treatment of novel coronavirus disease 2019 (COVID19) are not yet known. Several drug studies have focused on the renin–angiotensin system (RAS) and angiotensin-converting enzyme 2 (ACE2). Angiotensin (Ang) II levels were found to be high in patients infected with SARS-CoV-2.1,2 The virus enters the cell after it binds to ACE2, as an ACE2– virus complex. The virus may alter ACE2 function and render the enzyme dysfunctional.2 Because the virus targets ACE2, treatments for COVID-19 may also need to target ACE2. In phase I and II studies and several case reports, recombinant ACE2 has been reported to improve the clinical course of patients with COVID-19 by increasing Ang II degradation.3–5 Along with Ang II, Ang III, and Ang IV may be responsible for severe forms of COVID-19. Ang II, a potent vasoconstrictor, triggers oxidative stress and inflammation. ACE2 converts Ang II to Ang 1–7 and Ang I to Ang 1–9.6 Ang 1–9 is one of the major products of the ACE pathway and is converted to Ang 1–7 by ACE and neprilysin.6,7 ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), statins, and some oral antidiabetics cause ACE2 upregulation.8 ACE2 upregulation increases the degradation of Ang II to Ang 1–7 and alamandine.9 Alamandine is a vasodilator peptide with anti-inflammatory and antiproliferative effects.9 ACE2 upregulation and an increase in Ang 1–7 and Ang 1–9 cause vasodilation and alleviate inflammation.10–12 Thus, increasing ACE2 and Ang 1–7 may contribute to the treatment of hypertension and diabetes, two critical comorbidities of COVID-19.13 Although an increase in the degradation of Ang II occurs in patients using ACEIs, Ang II formation continues through secondary pathways. Cathepsin G and kallikrein enzymes produce Ang II independently of ACE.14 ACE also breaks down bradykinin and, when ACE is blocked, bradykinin levels increase.15 Bradykinin activates the chymase pathway in tissues such as the heart and lung,15 allowing production of Ang II, Ang III, and Ang IV. The chymase pathway also generates Ang II from Ang 1–12.14 According to the results of a meta-analysis, ACEIs and ARBs do not adversely affect mortality rate and duration of hospital stay in patients with COVID-19.16 The metaanalysis indicated that ACEIs have a protective effect against COVID-19, but ARBs do not.16 However, in patients using ACEIs, Ang II formation continues through non-ACE pathways. The existence of alternative pathways for Ang II production and the increased ","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320972019"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38584248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of ACEI and ARB on COVID-19 patients: A meta-analysis.","authors":"Yang Xue,&nbsp;Shaoqing Sun,&nbsp;Jianing Cai,&nbsp;Linwen Zeng,&nbsp;Shihui Wang,&nbsp;Suhuai Wang,&nbsp;Jingjie Li,&nbsp;Lin Sun,&nbsp;Jianmin Huo","doi":"10.1177/1470320320981321","DOIUrl":"https://doi.org/10.1177/1470320320981321","url":null,"abstract":"<p><strong>Background: </strong>The clinical use of angiotensin-converting enzyme inhibitors (ACEI) and angiotensin-receptor blockers (ARB) in patients with COVID-19 infection remains controversial. Therefore, we performed a meta-analysis on the effects of ACEI/ARB on disease symptoms and laboratory tests in hypertensive patients infected with COVID-19 virus and those who did not use ACEI/ARB.</p><p><strong>Methods: </strong>We systematically searched the relevant literatures from Pubmed, Embase, EuropePMC, CNKI, and other databases during the study period of 31 December 2019 (solstice, 15 March 2020), and analyzed the differences in symptoms and laboratory tests between patients with COVID-19 and hypertension who used ACEI/ARB drugs and those who did not. All statistical analyses were performed with REVMAN5.3.</p><p><strong>Results: </strong>We included a total of 1808 patients with hypertension diagnosed with COVID-19 in six studies. Analysis results show that ACEI/ARB drugs group D-dimer is lower (SMD = -0.22, 95%CI: -0.36 to -0.06), and the chances of getting fever is lower (OR = 0.74, 95%CI: 0.55 to 0.98). Meanwhile, laboratory data and symptoms were not statistical difference, but creatinine tends to rise (SMD = 0.22, 95% CI: 0.04 to 0.41).</p><p><strong>Conclusion: </strong>We found that the administration of ACEI/ARB drugs had positive effect on reducing D-dimer and the number of people with fever. Meanwhile it had no significant effect on other laboratory tests (creatinine excepted) or symptoms in patients with COVID-19, while special attention was still needed in patients with renal insufficiency.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320981321"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320981321","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38716092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haplotype-based association study between PRCP gene polymorphisms and essential hypertension in Hani minority group from a remote region of China.","authors":"Yanrui Wu,&nbsp;Xingming Pan,&nbsp;Xiaoxiao Jin","doi":"10.1177/1470320320981316","DOIUrl":"https://doi.org/10.1177/1470320320981316","url":null,"abstract":"<p><strong>Objective: </strong>Prolylcarboxypeptidase (PRCP) is both involved in the Kallikrein-Kinin system (KKS) and renin-angiotensin-aldosterone system (RAAS). This study aimed to determine the genetic impact of PRCP gene polymorphisms on essential hypertension (EH) in an isolated population from a remote region of China.</p><p><strong>Methods: </strong>A haplotype-based study was investigated in 346 EH patients and 346 normal subjects and all samples were Hani minority residents in Southwest China. A total of 11 tag single nucleotide polymorphisms (SNPs) in PRCP gene were tested by polymerase chain reaction-restriction fragment length polymorphism method.</p><p><strong>Results: </strong>Single site analysis found that PRCP gene 3'UTR SNP rs3750931 was associated with EH. The minor allele G of rs3750931 was more prevalent in the EH patients compared to control subjects after Bonferroni correction (<i>p</i> < 0.05). Moreover, the rs3750931 G allele carriers showed higher average blood pressure (BP) level among the subjects. The H2 (GAGCACTAACA) haplotype without rs3750931 G allele showed the protective effect for EH (OR = 0.68, 95 CI 0.54-0.85, <i>p</i> = 0.001).</p><p><strong>Conclusion: </strong>The present study indicated PRCP gene rs3750931 was associated with the risk of EH. This SNP G allele could be considered as one of risk markers for EH in Hani population.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320981316"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320981316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38710851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The value of the post-captopril aldosterone/renin ratio for the diagnosis of primary aldosteronism and the influential factors: A meta-analysis.","authors":"Qiao Xiang,&nbsp;Wen Wang,&nbsp;Tao Chen,&nbsp;Kai Yu,&nbsp;Qianrui Li,&nbsp;Tingting Zhang,&nbsp;Haoming Tian,&nbsp;Yan Ren","doi":"10.1177/1470320320972032","DOIUrl":"https://doi.org/10.1177/1470320320972032","url":null,"abstract":"<p><strong>Objective: </strong>The procedure for the captopril challenge test (CCT) in diagnosing primary aldosteronism (PA) is not standardized. We performed a meta-analysis to evaluate the controversial diagnostic value and influential factors of the post-captopril aldosterone/renin ratio (ARR).</p><p><strong>Methods: </strong>We searched literature in databases for eligible studies (until October 1, 2020). We extracted information regarding study and patient characteristics, CCT methods, outcome data. We pooled studies using the random-effect model. We performed meta-regression and six pre-specified subgroup analyses to explore heterogeneity.</p><p><strong>Results: </strong>Nineteen studies involving 4568 subjects were included. The pooled sensitivity and specificity were 0.825 (95% CI 0.804-0.844) and 0.919 (95% CI 0.908-0.928). The area under the summary receiver operating characteristic curve was 0.9487 (95% CI 0.9207-0.9767). Meta-regression revealed that heterogeneity might derive from time interval (<i>p</i> = 0.0117) and study population (<i>p</i> = 0.0033). Subgroup analyses showed significant differences between the subgroups stratified by the dose, posture, study region, time interval, cut-off value and study population for sensitivity and/or specificity (<i>p</i> < 0.05).</p><p><strong>Conclusion: </strong>Post-captopril ARR is comparably valuable for diagnosing PA at cut-offs from 12.0 to 50.0. Conducting the CCT in the supine position with 25 mg of captopril may attain greater sensitivity. Conducting the CCT in the seated position with 50 mg of captopril may attain greater specificity. A 90-min time interval may perform best in both the sensitivity and specificity.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320972032"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38641969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Central involvement of SARS-CoV-2 may aggravate ARDS and hypertension.","authors":"Erkan Cure,&nbsp;Medine Cumhur Cure,&nbsp;Hulya Vatansev","doi":"10.1177/1470320320972015","DOIUrl":"https://doi.org/10.1177/1470320320972015","url":null,"abstract":"Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Dear Sir, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to spread rapidly all over the world; however, the mechanism of the disease is not yet fully understood. Why do many people who come into contact with the virus not get sick and remain asymptomatic? Why do some people recover with tiny symptoms, while other people have a severe infection or die? SARSCoV-2 infection can lead to severe or fatal outcomes in patients with comorbid diseases such as hypertension, diabetes, obesity, and heart failure. SARS-CoV-2 binds to angiotensin-converting enzyme (ACE)-2, like SARS-CoV, enters the cells and causes infection. The renin-angiotensin system (RAS) plays a crucial role in the virus entry to cells and the progression of the virus-induced disease. Whether ACE2 upregulation will increase viral load remains unclear.1 ACE2 up-regulation increases angiotensin 1–7 formation and may have a protective effect against SARSCOV-2 caused acute respiratory distress syndrome (ARDS) and heart damage.1 Angiotensin II level is high in patients with the novel coronavirus disease 2019 (COVID19). According to an extensive view, SARS-CoV-2 binds to ACE2, causing ACE2 to become dysfunctional.2 Therefore, increased angiotensin II level leads to ARDS and heart damage.2 Interestingly, most infected people have no symptoms, and they do not have heart or lung damage. The effects of SARS-CoV-2 on peripheral RAS have been highlighted so far. We believe that the central RAS involvement of the virus has vital implications for COVID-19 progression. Regulation of pulmonary vascular tone is vital for the maintenance of pulmonary functions. RAS regulates vasoconstriction and vasodilation of the pulmonary vascular system. Bradykinin and kinin are responsible for the permeability and vasodilation of the pulmonary vascular system (Figure 1). Inflammation leads to an increase in bradykinin-1 receptor (B1R) in the lungs. They increase vascular permeability by binding bradykinin to the bradykinin-2 receptor (B2R) and des-arg9-bradykinin binding to the B1R. Increased pulmonary vascular permeability causes pulmonary edema.3,4 SARS-CoV-2 can cause ARDS via the bradykinin pathway in the lung (Figure 1).3,4 The brain is one of the tissues containing ACE2, such as the lung, heart, pancreas, kidney, and vascular endothelium, and SARS-CoV-2 can easily infect the brain.5,6 The virus infects the brain after can cross the blood-brain barrier either by direct transport through the bloodstream or indirectly by binding to the vascular endotheliu","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320972015"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38592575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of contrast-induced acute kidney injury on the association between renin-angiotensin system inhibitors and long-term mortality in heart failure patients.","authors":"Li Lei,&nbsp;Yulu Huang,&nbsp;Zhaodong Guo,&nbsp;Feier Song,&nbsp;Yibo He,&nbsp;Jin Liu,&nbsp;Guoli Sun,&nbsp;Bowen Liu,&nbsp;Pengyuan Chen,&nbsp;Jianbin Zhao,&nbsp;Dengxuan Wu,&nbsp;Yan Xue,&nbsp;Wenhe Yan,&nbsp;Zefeng Lin,&nbsp;Xiuqiong Huang,&nbsp;Guanzhong Chen,&nbsp;Shiqun Chen,&nbsp;Yong Liu,&nbsp;Jiyan Chen","doi":"10.1177/1470320320979795","DOIUrl":"https://doi.org/10.1177/1470320320979795","url":null,"abstract":"<p><strong>Introduction: </strong>Renin-angiotensin system inhibitors (RASi) reduce mortality among heart failure (HF) patients, but their effect among those complicating contrast-induced acute kidney injury (CI-AKI) remains unexplored. We aimed to investigate whether the relationship between RASi prescription at discharge and mortality differs between HF patients with or without CI-AKI following coronary angiography (CAG).</p><p><strong>Methods: </strong>About 596 HF patients from an observational cohort were divided into a CI-AKI group (<i>n</i> = 104) and a non-CI-AKI group (<i>n</i> = 492) based on whether they had CI-AKI following CAG. The endpoint was all-cause mortality. Multivariable Cox regression was performed in each group to explore the associations between RASi at discharge and mortality.</p><p><strong>Results: </strong>During the median follow-up time of 2.26 (1.70; 3.24) years, higher mortality rate was observed in the CI-AKI group compared to the non-CI-AKI group (18.3% vs 8.9%, <i>p</i> = 0.002). Among HF patients with CI-AKI, after adjusting for confounding factors, the association was not significant between RASi prescription at discharge and mortality (HR: 0.39, 95%CI: 0.12-1.31, <i>p</i> = 0.128), while it was among those without CI-AKI (HR: 0.39, 95%CI: 0.18-0.84, <i>p</i> = 0.016).</p><p><strong>Conclusion: </strong>RASi prescription at discharge for HF patients complicating CI-AKI tended to be ineffective, while it benefited those without CI-AKI. Further randomized evidence is needed to confirm this trend.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320979795"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320979795","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38373375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Countermeasure and therapeutic: A(1-7) to treat acute respiratory distress syndrome due to COVID-19 infection.","authors":"Maira Soto,&nbsp;Gere diZerega,&nbsp;Kathleen E Rodgers","doi":"10.1177/1470320320972018","DOIUrl":"https://doi.org/10.1177/1470320320972018","url":null,"abstract":"<p><p>In the wake of the COVID-19 pandemic it has become clear that there is a need for therapies that are capable of reducing damage caused to patients from infections. Infections that induce Acute Respiratory Distress Syndrome (ARDS) are especially devastating because lung damage is so critical and difficult to manage. Angiotensin (1-7) [A(1-7)] has already been shown to protect pulmonary health and architecture in various models of disease. There is also evidence that A(1-7) can modulate immune function and protect various organs (lung, kidney, and heart) from oxidative damage and inflammation. Here we focus on making a case for the development of novel therapies that target the protective arm of the Renin Angiotensin System (RAS).</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320972018"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320972018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38689219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads.","authors":"Martijn Hoevenaar, Dolf Goossens, Janne Roorda","doi":"10.1177/1470320320979097","DOIUrl":"10.1177/1470320320979097","url":null,"abstract":"<p><p>Because of the current COVID-19-pandemic, the world is currently being held hostage in various lockdowns. ACE2 facilitates SARS-CoV-2 cell-entry, and is at the very center of several pathophysiological pathways regarding the RAAS, CS, KKS, T2DM, and IL-6. Their interactions with severe COVID-19 complications (e.g. ARDS and thrombosis), and potential therapeutic targets for pharmacological intervention, will be reviewed.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320979097"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320979097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38343724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genetic polymorphisms of angiotensin converting enzyme insertion/deletion and glioma susceptibility: A meta-analysis.","authors":"Meili Sun,&nbsp;Yuying Fang,&nbsp;Shuzhen Ma,&nbsp;Ximei Gao,&nbsp;Yuping Sun","doi":"10.1177/1470320320963939","DOIUrl":"https://doi.org/10.1177/1470320320963939","url":null,"abstract":"<p><strong>Objective: </strong>The previous studies on angiotensin converting enzyme (ACE) insertion/deletion (I/D) genetic polymorphism and glioma risk were inconsistent. Therefore, we performed a meta-analysis to assess the association between ACE I/D polymorphisms and glioma risk.</p><p><strong>Methods and results: </strong>In total, four populations (1110 cases and 1335 controls) on ACE I/D polymorphism were included. Overall, the meta-analysis demonstrated no significant association between ACE I/D polymorphism and glioma risk. In addition, the analysis of the association of ACE I/D polymorphism and clinical grade also showed no significant association.</p><p><strong>Conclusion: </strong>Our meta-analysis didn't find a significant association between ACE I/D polymorphism glioma risk. However, further studies with larger sample size and more ethnic groups are required to confirm the results.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320963939"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/1470320320963939","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38478908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensinogen M235T polymorphism and susceptibility to hypertrophic cardiomyopathy in Asian population: A meta analysis.","authors":"Zhen Zhen, Lu Gao, Qin Wang, Xi Chen, Jia Na, Xiwei Xu, Yue Yuan","doi":"10.1177/1470320320978100","DOIUrl":"10.1177/1470320320978100","url":null,"abstract":"<p><strong>Objective: </strong>To explore the relationship between the polymorphism of angiotensinogen gene (AGT) M235T and susceptibility to hypertrophic cardiomyopathy (HCM) in Asian population by meta-analysis.</p><p><strong>Methods: </strong>PubMed, Embase, Web of Science, Cochrane library, CNKI, Wan Fang, and other databases were searched to collect the literature about AGT M235T polymorphism and HCM from the inception to March 1, 2020. The Newcastle-Ottawa Scale (NOS) checklist was uesd to perform independent literature review and study quality assessment. Data was analyzed by Stata 15.0 software.</p><p><strong>Results: </strong>The results showed that, except for the recessive genetic model (TT vs MT+MM: OR = 1.27, 95%CI: 1.05-1.53), in the other four genetic models, the M235T polymorphism had no significant correlation with the risk of HCM (T vs M: OR = 1.17, 95%CI: 0.88-1.57; TT+MT vs MM: OR = 1.13, 95%CI: 0.55-2.33; TT vs MM: OR = 1.25, 95%CI: 0.60-2.59; TM vs MM: OR = 0.95, 95%CI0.5-1.82). The results of subgroup analysis showed that, except for the heterozygous genetic model, in the other four genetic models, M235T polymorphism was significantly associated with sporadic hypertrophic cardiomyopathy (SHCM), but not with familial hypertrophic cardiomyopathy (FHCM) (<i>p</i> > 0.05).</p><p><strong>Conclusion: </strong>M235T polymorphism in Asians is associated with HCM, especially SHCM. Heterozygotes increase the risk of patients with SHCM.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"21 4","pages":"1470320320978100"},"PeriodicalIF":2.9,"publicationDate":"2020-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5b/43/10.1177_1470320320978100.PMC7734517.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38696739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}