Evidence map›Paper›PMID 33424337›Full record

ArticleSaudi journal of biological sciences2021

Diabetes induced renal complications by leukocyte activation of nuclear factor κ-B and its regulated genes expression.

Noura M Darwish, Yousif M Elnahas, Fatmah S AlQahtany

Open access · hybridAbstract read
In one paragraph

Article in Saudi journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. High glucose induces pro-inflammatory polarization of macrophages by inhibiting immune-responsive gene 1 expression.Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Effects ofReports of biochemistry & molecular biology · 2021
    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

3 authors at 2 institutions in 2 countries.

Noura M DarwishDepartment of Biochemistry, Faculty of Science, Ain Shams University, 11566, Egypt.
Yousif M ElnahasDepartment of Surgery, College of Medicine, King Saud University, Medical City, Riyadh 24251, Saudi Arabia.
Fatmah S AlQahtanyDepartment of Pathology, Hematopathology Unit, College of Medicine, King Saud University, Medical City, King Saud University, Riyadh 24251, Saudi Arabia.
King Saud University · SAAin Shams University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2D) is a metabolic disorder characterized by inappropriate insulin function. Despite wide progress in genome studies, defects in gene expression for diabetes prognosis still incompletely identified. Prolonged hyperglycemia activates NF-κB, which is a main player in vascular dysfunctions of diabetes. Activated NF-κB, triggers expression of various genes that promote inflammation and cell adhesion process. Alteration of pro-inflammatory and profibrotic gene expression contribute to the irreversible functional and structural changes in the kidney resulting in diabetic nephropathy (DN). To identify the effect of some important NF-κB related genes on mediation of DN progression, we divided our candidate genes on the basis of their function exerted in bloodstream into three categories (Proinflammatory; NF-κB, IL-1B, IL-6, TNF-α and VEGF); (Profibrotic; FN, ICAM-1, VCAM-1) and (Proliferative; MAPK-1 and EGF). We analyzed their expression profile in leukocytes of patients and explored their correlation to diabetic kidney injury features. Our data revealed the overexpression of both proinflammatory and profibrotic genes in DN group when compared to T2D group and were associated positively with each other in DN group indicating their possible role in DN progression. In DN patients, increased expression of proinflammatory genes correlated positively with glycemic control and inflammatory markers indicating their role in DN progression. Our data revealed that the persistent activation NF-κB and its related genes observed in hyperglycemia might contribute to DN progression and might be a good diagnostic and therapeutic target for DN progression. Large-scale studies are needed to evaluate the potential of these molecules to serve as disease biomarkers.

Indexed as

2hPPBG, 2 h post prandial blood glucose.ACR, albumin creatinine ratioBMI, body mass index.DBP, Diastolic blood pressure.DN, diabetic nephropathy.e-GFR, estimated glomerular filtration rate.FBS, fasting blood glucose.FNHbA1c, Glycosylated hemoglobin.HDL, High density lipoprotein-cholesterol.ICAM-1IL-1βIL-6LDL, Low density lipoprotein-cholesterol.M, male, F, female.NF-κBSBP, Systolic blood pressure.S.Cr, serum creatinine.T2D, type 2 diabetes mellitus without nephropathy.TC, total cholesterol.TGs, Triglyceride.TNF-αVCAM-1VEGFVLDL, Very low-density lipoprotein.

Identifiers

PMID33424337
PMCPMC7783672
OpenAlexW3081691570

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.