Evidence map›Paper›PMID 36557328›Full record

ReviewMetabolites2022

Genetic Polymorphism in Angiotensinogen and Its Association with Cardiometabolic Diseases.

Momina Shahid, Kanwal Rehman, Muhammad Sajid Hamid Akash, Shaleem Suhail, Shagufta Kamal, Muhammad Imran, Mohammed A Assiri

Open access · goldAbstract readReview
In one paragraph

Review in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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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

7 authors at 4 institutions in 2 countries.

Momina ShahidDepartment of Pharmaceutical Chemistry, Government College University, Faisalabad 38000, Pakistan.
Kanwal RehmanDepartment of Pharmacy, The Women University, Multan 60000, Pakistan.ORCID 0000-0001-7873-6681
Muhammad Sajid Hamid AkashDepartment of Pharmaceutical Chemistry, Government College University, Faisalabad 38000, Pakistan.ORCID 0000-0002-9446-5233
Shaleem SuhailDepartment of Pharmacy, University of Chenab, Gujrat 50700, Pakistan.
Shagufta KamalDepartment of Biochemistry, Government College University, Faisalabad 38000, Pakistan.
Muhammad ImranResearch Center for Advanced Materials Science (RCAMS), King Khalid University, Abha 61514, Saudi Arabia.ORCID 0000-0003-4072-4997
Mohammed A AssiriResearch Center for Advanced Materials Science (RCAMS), King Khalid University, Abha 61514, Saudi Arabia.
Government College University, Faisalabad · PKKing Khalid University · SAThe University of Chenab, GujratThe Women University Multan · PK

Funding

the Deanship of Scientific Research at King Khalid University Saudi Arabia for funding through the research groups program R.G.P.2/170/43
6 · The paper itself

Abstract

Angiotensinogen (AGT) is one of the most significant enzymes of the renin-angiotensin-aldosterone system (RAAS) which is involved in the regulation and maintenance of blood pressure. AGT is involved in the production of angiotensin I which is then converted into angiotensin II that leads to renal homeostasis. However, various genetic polymorphisms in AGT have been discovered in recent times which have shown an association with various diseases. Genetic polymorphism increases the level of circulating AGT in blood which exaggerates the effects produced by AGT. The associated diseases occur due to various effects produced by increased AGT levels. Several cardiovascular diseases including myocardial infarction, coronary heart disease, heart failure, hypertrophy, etc. are associated with AGT polymorphism. Other diseases such as depression, obesity, diabetic nephropathy, pre-eclampsia, and liver injury are also associated with some variants of AGT gene. The most common variants of AGT polymorphism are M235T and T174M. The two variants are associated with many diseases. Some other variants such as G-217A, A-6G, A-20C and G-152A, are also present but they are not as significant as that of M235T and T174M variants. These variants increase the level of circulating AGT and are associated with prevalence of different diseases. These diseases occur through various pathological pathways, but the initial reason remains the same, i.e., increased level of AGT in the blood. In this article, we have majorly focused on how genetic polymorphism of different variants of AGT gene is associated with the prevalence of different diseases.

Indexed as

A-20CA-6GAGT polymorphismassociated diseasesG-152AG-217AM235TT174M

Identifiers

PMID36557328
PMCPMC9785123
OpenAlexW4312212267

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.