Evidence map›Paper›PMID 37143982›Full record

ArticleFrontiers in public health2023

Common gene signatures and molecular mechanisms of diabetic nephropathy and metabolic syndrome.

Chengyu Zhang, Han Li, Shixiang Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in public health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 11 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

3 authors at 2 institutions in 1 country.

Chengyu ZhangDepartment of Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Han LiDepartment of Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Shixiang WangDepartment of Nephrology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Multiple metabolic toxicities, redox stress, and endothelial dysfunction contribute to the development of diabetic glomerulosclerosis and DN. Metabolic syndrome (MetS) is a pathological state in which the body's ability to process carbohydrates, fats, and proteins is compromised because of metabolic disorders, resulting in redox stress and renal remodeling. However, a causal relationship between MetS and DN has not been proven. This study aimed to provide valuable information for the clinical diagnosis and treatment of MetS with DN. Methods: Here, transcriptome data of DN and MetS patients were obtained from the Gene Expression Omnibus database, and seven potential biomarkers were screened using bioinformatics analysis. In addition, the relationship between these marker genes and metabolism and immune infiltration was explored. Among the identified marker genes, the relationship between Results: We found that Conclusion: Overall, our findings can aid in further investigation of the effects of drug treatment on single cells of patients with diabetes to validate PLEKHA1 as a therapeutic target and to inform the development of targeted therapies.

Indexed as

Diabetes MellitusDiabetic NephropathiesMetabolic SyndromeBiomarkersEndothelial CellsHumansKidneyBiomarkersdiabetic nephropathyoxidative phosphorylationsingle-cell analysistranscription datatype 2 diabetes

Identifiers

PMID37143982
PMCPMC10151256
OpenAlexW4361277816

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.