Evidence map›Paper›PMID 28120210›Full record

ArticleMolecular and cellular biochemistry2017

Renin-angiotensin system gene polymorphisms as potential modifiers of hypertrophic and dilated cardiomyopathy phenotypes.

Bindu Rani, Amit Kumar, Ajay Bahl, Rajni Sharma, Rishikesh Prasad, Madhu Khullar

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In one paragraph

Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 4 pooled it
1.4field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 4 syntheses or guidelines pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Article
  7. Article
  8. Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019
    Review
  9. Pediatric Cardiomyopathies.Circulation research · 2017
    Review
  10. Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Bindu RaniDepartment of Experimental Medicine and Biotechnology, PGIMER, Lab No 2009, Research Block B, Chandigarh, 160012, India.
Amit KumarDepartment of Experimental Medicine and Biotechnology, PGIMER, Lab No 2009, Research Block B, Chandigarh, 160012, India.
Ajay BahlDepartment of Cardiology, PGIMER, Chandigarh, India.
Rajni SharmaDepartment of Otolaryngology, PGIMER, Chandigarh, India.
Rishikesh PrasadDepartment of Experimental Medicine and Biotechnology, PGIMER, Lab No 2009, Research Block B, Chandigarh, 160012, India.
Madhu KhullarDepartment of Experimental Medicine and Biotechnology, PGIMER, Lab No 2009, Research Block B, Chandigarh, 160012, India. madhu.khullar@gmail.com.
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The renin-angiotensin (RAS) pathway has an important role in the etiology of heart failure and given the importance of RAS as a therapeutic target in various cardiomyopathies, genetic polymorphisms in the RAS genes may modulate the risk and severity of disease in cardiomyopathy patients. In the present study, we examined the association of RAS pathway gene polymorphisms, angiotensin converting enzyme (ACE), angiotensinogen (AGT), and angiotensin receptor type 1 (AGTR1) with risk and disease severity in Asian Indian idiopathic cardiomyopathy patients. The case-control study was conducted in 400 cardiomyopathy patients diagnosed with HCM, DCM, or restrictive cardiomyopathy (RCM) and 235 healthy controls. Genotyping of patients and controls was done by PCR-RFLP assays. Left ventricular wall thickness and left ventricular ejection fraction were measured by means of M-mode echocardiography. We observed significantly higher prevalence of ACE DD and AGTR1 1166CC genotypes in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) patients. Also, 235TT genotype of AGT (M235T) was significantly associated with enhanced risk of the disease phenotype in HCM, DCM, and RCM.

Indexed as

Polymorphism, Restriction Fragment LengthAdultAngiotensinogenCardiomyopathy, DilatedCardiomyopathy, HypertrophicFemaleHumansMaleMiddle AgedPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1Renin-Angiotensin SystemACE protein, humanAGTR1 protein, humanAngiotensinogenPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1AngiotensinogenHypertrophyIdiopathic cardiomyopathiesModifier genesSingle nucleotide polymorphisms

Identifiers

PMID28120210
OpenAlexW2580625675

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.