Evidence map›Paper›PMID 37493735›Full record

ArticleRevista da Sociedade Brasileira de Medicina Tropical2023

Association of PI3K/AKT/mTOR pathway autophagy-related gene polymorphisms with pulmonary tuberculosis susceptibility in a Chinese population.

Juan He, Shengyuan Liu, Xujun Guo, Fan Zhang, Yuzheng Fan, Lijuan Wu, Howard Eugene Takiff, Yashuang Zhao

Open access · diamondAbstract read
In one paragraph

Article in Revista da Sociedade Brasileira de Medicina Tropical, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 4 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

8 authors at 2 institutions in 1 country.

Juan HeHarbin Medical University, School of Public Health, Department of Epidemiology, Harbin, China.ORCID http://orcid.org/0000-0002-7355-7227
Shengyuan LiuShenzhen Nanshan Center for Chronic Disease Control, Department of Tuberculosis Control and Prevention, Shenzhen, China.ORCID http://orcid.org/0000-0001-5494-7660
Xujun GuoShenzhen Nanshan Center for Chronic Disease Control, Department of Tuberculosis Control and Prevention, Shenzhen, China.ORCID http://orcid.org/0000-0002-9047-1142
Fan ZhangShenzhen Nanshan Center for Chronic Disease Control, Department of Tuberculosis Control and Prevention, Shenzhen, China.ORCID http://orcid.org/0009-0002-0791-422X
Yuzheng FanShenzhen Nanshan Center for Chronic Disease Control, Department of Tuberculosis Control and Prevention, Shenzhen, China.ORCID http://orcid.org/0000-0002-1338-8652
Lijuan WuShenzhen Nanshan Center for Chronic Disease Control, Department of Tuberculosis Control and Prevention, Shenzhen, China.ORCID http://orcid.org/0009-0002-1827-6817
Howard Eugene TakiffLaboratorio de Genética Molecular, CMBC, IVIC, Caracas, Venezuela.ORCID http://orcid.org/0000-0002-0480-0860
Yashuang ZhaoHarbin Medical University, School of Public Health, Department of Epidemiology, Harbin, China.ORCID http://orcid.org/0000-0002-7425-5773
Shenzhen Nanshan Center for Chronic Disease Control · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutophagy can inhibit the survival of intracellular microorganisms including Mycobacterium tuberculosis (Mtb), and the PI3K/AKT/mTOR pathway plays a crucial role. This study investigated the association between PI3K/AKT/mTOR pathway autophagy-related gene polymorphisms and pulmonary tuberculosis (PTB) susceptibility.

methodsKEGG pathway and gene ontology (GO) databases were searched for genes belonging to the PI3K/AKT/mTOR and autophagy pathways. Thirty SNPs in nine genes were identified and tested for their associations with tuberculosis in 130 patients with PTB and 271 controls. We constructed genetic risk scores (GRSs) and divided the participants into 3 subgroups based on their GRSs:0-5, 6-10, and 11-16.

resultsThis analysis revealed that the AKT1 (rs12432802), RPTOR (rs11654508, rs12602885, rs2090204, rs2589144, and rs2672897), and TSC2 (rs2074969) polymorphisms were significantly associated with PTB risk. A decreasing trend was observed (P trend 0.020), in which a lower GRS was associated with a higher risk of PTB ([6-10] vs. [0-5]: OR (95%CI) 0.590 (0.374-0.931); [11-16] vs. [0-5]: OR (95%CI) 0.381 (0.160-0.906)).

conclusionsPolymorphisms in AKT1, RPTOR, and TSC2 may influence susceptibility to PTB.

Indexed as

AutophagyProto-Oncogene Proteins c-aktTuberculosis, PulmonaryCase-Control StudiesEast Asian PeopleGenetic Predisposition to DiseaseHumansPhosphatidylinositol 3-KinasesPolymorphism, Single NucleotideRegulatory-Associated Protein of mTORTOR Serine-Threonine KinasesTuberous Sclerosis Complex 2 ProteinAKT1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRegulatory-Associated Protein of mTORRPTOR protein, humanTOR Serine-Threonine KinasesTSC2 protein, humanTuberous Sclerosis Complex 2 Protein

Identifiers

PMID37493735
PMCPMC10367219
OpenAlexW4385169485

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.