Evidence map›Paper›PMID 40937328›Full record

ArticleBiochemistry and biophysics reports2025

LncRNAs IFNG-AS1 and TH2LCRR as potential biomarkers of Th1/Th2 imbalance in diabetic nephropathy: From bioinformatics to experimental validation.

Seyed Amir Hossein Hosseini, Parisa Ajorlou, Maryam Salehian, Aghdas Dehghani

Abstract read
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Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

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0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. CD4Frontiers in immunology · 2026
    Review
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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

4 authors.

Seyed Amir Hossein HosseiniEndocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Parisa AjorlouEndocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Maryam SalehianDepartment of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran.
Aghdas DehghaniEndocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The inflammatory response is a pivotal mechanism underlying the progression of type 2 diabetes mellitus (T2DM) into diabetic nephropathy (DN). Upstream lncRNAs regulate inflammatory molecules, and their dysregulation can disrupt immune homeostasis. Th1/Th2 imbalance is one of the most significant causes of DN progression. This research aims to uncover novel biomarkers and elucidate the underlying molecular mechanisms involved in DN. Methods: The GSE135390 dataset was analyzed to identify differentially expressed genes (DEGs) associated with Th1 cell differentiation. Based on literature review and NcPath databases, IFNG-AS1(Th1) and TH2LCRR (Th2) were selected as the top lncRNAs. To validate our bioinformatics findings, real-time PCR was conducted on 90 participants categorized into four groups: 30 with T2DM, 30 with DN (15 with microalbuminuria and 15 with ESRD), and 30 healthy controls. Results: The analysis of real-time PCR results revealed a notable upregulation in IFNG-AS1 expression in ESRD patients compared to individuals with T2DM and healthy controls. Moreover, a significant increase in IFNG-AS1 expression was observed in patients with microalbuminuria relative to healthy subjects. Conversely, TH2LCRR expression was notably reduced in patients with ESRD, microalbuminuria, and T2DM compared to healthy individuals. Expression of IFNG-AS1 and TH2LCRR showed strong correlation with biochemical markers, including HbA1c, ESR, BUN, GFR, and albumin. Conclusion: This study demonstrates the potential role of IFNG-AS1 and TH2LCRR as key regulators in the immunopathogenesis of DN. Their dysregulated expression may contribute to Th1/Th2 imbalance, providing a deeper understanding of immune-mediated mechanisms involved in DN progression.

Indexed as

BioinformaticsDiabetes nephropathyIFNG-AS1lncRNATh1Th2TH2LCRR

Identifiers

PMID40937328
PMCPMC12420516

What Socratic holds

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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 Socratic graph.