Evidence map›Paper›PMID 40671147›Full record

ArticleDiabetology & metabolic syndrome2025

Synergistic effects of NF-κB1 and inflammatory pathway polymorphisms on hypertension and dyslipidemia susceptibility in type 2 diabetes.

Chao Zuo, Jing Cheng, Dongli Yang, Yi Liu, Hailian Chen, Xiang Lu, Mengna Guo, Zhuo Yang, Ziqiang Wang, Yu Wang and 1 more

Abstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2025. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. 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

11 authors.

Chao Zuo *Department of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Jing Cheng *Department of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Dongli Yang *Department of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Yi LiuDepartment of Pathology, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Hailian ChenDepartment of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Xiang LuDepartment of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Mengna GuoDepartment of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Zhuo YangDepartment of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Ziqiang WangResearch Center of Clinical Laboratory Science, Bengbu Medical University, Bengbu, Anhui, China.
Yu WangDepartment of Geriatrics, The First Affiliated Hospital of Guilin Medical University, Le Qun Road 15, Guilin, 541001, Guangxi, China. wangyu101101@163.com.
Yongchao QiaoDepartment of Clinical Laboratory, The First Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China. qiaoyc@glmc.edu.cn.

Funding

the general program of Guangxi Natural Science Foundation 2025GXNSFHA069198the Guangxi medical and health appropriate technology development and application project S2024041the Innovation Project of Guangxi Graduate Education No. YCSW2024441the self-funded project of Guangxi Traditional Chinese Medicine GXZYC20230356
6 · The paper itself

Abstract

backgroundType 2 diabetes mellitus (T2DM) patients exhibit a heightened susceptibility to concurrent hypertension (HTN) and dyslipidemia (DYS), conditions that reciprocally exacerbate cardiovascular risks. This study investigated the association between NF-κB1 polymorphism, related inflammatory mediators, and the predisposition to hypertension and dyslipidemia in T2DM patients, along with their correlations with biochemical parameters.

methodsGenotyping of 452 T2DM patients was performed using SNP-scan high-throughput technology. Analyzed polymorphisms encompassed: NF-κB1-rs4648068, upstream transcriptional regulators (TLR2-rs3804099, TLR4-rs2149356, TLR9-rs352140), and downstream inflammatory mediators (IL6-rs1800796, IL6R-rs2228145, IL10-rs1800872, ICAM1-rs5498 and rs3093030). The cohort was stratified into three clinically defined groups: T2DM-only (T2DM group), T2DM with hypertension (T2MH group), and T2DM with comorbid hypertension and dyslipidemia (T2MH-DYS group). The T2MH and T2MH-DYS groups were further subclassified into Grade I-III according to hypertension staging criteria. Plasma biochemical profiles were systematically evaluated to delineate their associations with NF-κB1 pathway genetic variants.

resultsPatients with T2DM complicated by hypertension (T2MH) or hypertension with dyslipidemia (T2MH-DYS) exhibited distinct metabolic and inflammatory profiles. Genetic analyses revealed significant polymorphisms in inflammatory pathway genes (TLR9, TLR2, NF-κB1, IL6R) across subgroups. TLR9 rs352140 CT heterozygotes conferred a 2.8-2.94-fold increased risk of T2MH/T2MH-DYS, while NF-κB1 rs4648068 GG genotype reduced dyslipidemia risk by 64.8% (P = 0.004). Haplotype analysis identified synergistic effects: the TLR9/IL6R/NF-κB1 risk haplotype (G-C-T) increased hypertension risk 3.26-fold (P = 0.00069), and the IL10/TLR4/NF-κB1 protective haplotype (G-T-A) reduced dyslipidemia risk by 82% (P = 0.0063). IL10 rs1800872 TT genotype and TLR4 rs2149356 G allele were linked to dyslipidemia susceptibility in hypertensive diabetics.

conclusionThis study establishes that genetic variants in inflammatory pathways (TLR9, NF-κB1, IL6R) synergistically drive hypertension and dyslipidemia risks in T2DM.

Indexed as

DyslipidemiaHypertension classificationNF-κB1PolymorphismT2DM

Identifiers

PMID40671147
PMCPMC12269108

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.