PMID- 38034011
OWN - NLM
STAT- MEDLINE
DCOM- 20231204
LR  - 20240228
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 14
DP  - 2023
TI  - Integrative bioinformatics analysis of biomarkers and pathways for exploring the 
      mechanisms and molecular targets associated with pyroptosis in type 2 diabetes 
      mellitus.
PG  - 1207142
LID - 10.3389/fendo.2023.1207142 [doi]
LID - 1207142
AB  - INTRODUCTION: Research has shown that pyroptosis contributes greatly to the 
      progression of diabetes and its complications. However, the exact relationship 
      between this particular cell death process and the pathology of type 2 diabetes 
      mellitus (T2DM) remains unclear. In this study, we used bioinformatic tools to 
      identify the pyroptosis-related genes (PRGs) associated with T2DM and to analyze 
      their roles in the disease pathology. METHODS: Two microarray datasets, GSE7014 
      and GSE25724, were obtained from the GEO database and assessed for differentially 
      expressed genes (DEGs). The T2DM-associated DEGs that overlapped with 
      differentially expressed PRGs were noted as T2DM-PRGs. Subsequently, 25 T2DM-PRGs 
      were validated and subjected to functional enrichment analysis through Gene 
      Ontology annotation analysis, Kyoto Encyclopedia of Genes and Genomes pathway 
      analysis, and gene set enrichment analysis (GSEA). The diagnostic and predictive 
      value of the T2DM-PRGs was evaluated using receiver operating characteristic 
      curves (ROC). Additionally, a single-sample GSEA algorithm was applied to study 
      immune infiltration in T2DM and assess immune infiltration levels. RESULTS: We 
      identified 25 T2DM-PRGs that were significantly enriched in the nuclear 
      factor-kappa B signaling and prostate cancer pathways. The top five 
      differentially expressed prognostic T2DM-PRGs targeted by miRNAs were PTEN, BRD4, 
      HSP90AB1, VIM, and PKN2. The top five differentially expressed T2DM-PRGs 
      associated with transcription factors were HSP90AB1, VIM, PLCG1, SCAF11, and 
      PTEN. The genes PLCG1, PTEN, TP63, CHI3L1, SDHB, DPP8, BCL2, SERPINB1, ACE2, 
      DRD2, DDX58, and BTK showed excellent diagnostic performance. The immune 
      infiltration analysis revealed notable differences in immune cells between T2DM 
      and normal tissues in both datasets. These findings suggest that T2DM-PRGs play a 
      crucial role in the development and progression of T2DM and could be used as 
      potential diagnostic biomarkers and therapeutic targets. DISCUSSION: 
      Investigating the mechanisms and biomarkers associated with pyroptosis may offer 
      valuable insights into the pathophysiology of T2DM and lead to novel therapeutic 
      approaches to treat the disease.
CI  - Copyright (c) 2023 Wang and Wang.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Endocrinology, School of Medicine, Zhongda Hospital, Institute of 
      Diabetes, Southeast University, Nanjing, Jiangsu, China.
AD  - Department of Endocrinology, First Affiliated Hospital of Baotou Medical Collage, 
      Baotou, China.
FAU - Wang, Yao
AU  - Wang Y
AD  - Department of Endocrinology, School of Medicine, Zhongda Hospital, Institute of 
      Diabetes, Southeast University, Nanjing, Jiangsu, China.
LA  - eng
PT  - Journal Article
DEP - 20231115
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
RN  - 0 (Nuclear Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (Biomarkers)
RN  - 147416-07-7 (SERPINB1 protein, human)
RN  - 0 (Serpins)
RN  - 0 (BRD4 protein, human)
RN  - 0 (Cell Cycle Proteins)
SB  - IM
MH  - Male
MH  - Humans
MH  - *Diabetes Mellitus, Type 2/genetics
MH  - Pyroptosis/genetics
MH  - Nuclear Proteins
MH  - Transcription Factors
MH  - Biomarkers
MH  - Computational Biology
MH  - *Serpins
MH  - Cell Cycle Proteins
PMC - PMC10684677
OTO - NOTNLM
OT  - biomarkers
OT  - diabetes mellitus
OT  - immune infiltration
OT  - mechanisms
OT  - pyroptosis
OT  - risk prediction
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/11/30 18:45
MHDA- 2023/12/04 12:41
PMCR- 2023/01/01
CRDT- 2023/11/30 17:27
PHST- 2023/04/17 00:00 [received]
PHST- 2023/10/30 00:00 [accepted]
PHST- 2023/12/04 12:41 [medline]
PHST- 2023/11/30 18:45 [pubmed]
PHST- 2023/11/30 17:27 [entrez]
PHST- 2023/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2023.1207142 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2023 Nov 15;14:1207142. doi: 
      10.3389/fendo.2023.1207142. eCollection 2023.