TGF-β/Smad signaling pathway in fatty liver disease: a case-control study.
Humans
Signal Transduction
Male
Case-Control Studies
Female
Middle Aged
Adult
Smad2 Protein
/ metabolism
Smad3 Protein
/ metabolism
Connective Tissue Growth Factor
/ genetics
Transforming Growth Factor beta1
/ metabolism
Fatty Liver
/ metabolism
Transforming Growth Factor beta
/ metabolism
Smad Proteins
/ metabolism
Non-alcoholic Fatty Liver Disease
/ metabolism
Transforming Growth Factor beta3
/ metabolism
Gene Expression Regulation
MAFLD
P-smad2/3
Smad2/3
TGF-β1
TGF-β3
non-MAFLD
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
01 Oct 2024
01 Oct 2024
Historique:
received:
11
09
2024
accepted:
24
09
2024
medline:
1
10
2024
pubmed:
1
10
2024
entrez:
1
10
2024
Statut:
epublish
Résumé
Fatty liver disease is a metabolic disorder that recently has been classified into two categories: metabolic dysfunction-associated fatty liver disease (MAFLD) and non-MAFLD. TGF-β signaling pathway is likely a significant factor in the pathogenesis of this condition, exerting its effects through its downstream signaling proteins, Smad2/3. Accordingly, this study aimed to investigate the TGF-β signaling pathway in the white blood cells (WBCs) of patients with MAFLD compared to those with non-MAFLD and control groups. In this study, 41 patients with fatty liver were evaluated, comprising 22 patients with MAFLD and 19 patients with non-MAFLD, and compared to 22 healthy controls. Gene expression of TGF-β1, TGF-β3, and CTGF were quantified using qRT-PCR, and the protein expressions of Smad2/3 and P-Smad2/3 were analyzed using western blotting. Gene expression analysis revealed a significant decrease in the gene expressions of the TGF-β1 and TGF-β3 and an increase in CTGF gene expression in patients with MAFLD and non-MAFLD compared to the control group. Notably, the Smad2/3 protein expression was significantly higher in the non-MAFLD group compared to the control group (P < 0.05). On the other hand, the P-smad2/3 protein expression was significantly elevated in the MAFLD group compared to the control group (P < 0.001). TGF-β signaling pathway in WBCs of patients with fatty liver are affected by a complex signaling pathway. However, metabolic factors most probably affect TGF-β1 gene expression and its downstream signaling proteins more than TGF-β3.
Sections du résumé
BACKGROUND
BACKGROUND
Fatty liver disease is a metabolic disorder that recently has been classified into two categories: metabolic dysfunction-associated fatty liver disease (MAFLD) and non-MAFLD. TGF-β signaling pathway is likely a significant factor in the pathogenesis of this condition, exerting its effects through its downstream signaling proteins, Smad2/3. Accordingly, this study aimed to investigate the TGF-β signaling pathway in the white blood cells (WBCs) of patients with MAFLD compared to those with non-MAFLD and control groups.
METHODS AND RESULTS
RESULTS
In this study, 41 patients with fatty liver were evaluated, comprising 22 patients with MAFLD and 19 patients with non-MAFLD, and compared to 22 healthy controls. Gene expression of TGF-β1, TGF-β3, and CTGF were quantified using qRT-PCR, and the protein expressions of Smad2/3 and P-Smad2/3 were analyzed using western blotting. Gene expression analysis revealed a significant decrease in the gene expressions of the TGF-β1 and TGF-β3 and an increase in CTGF gene expression in patients with MAFLD and non-MAFLD compared to the control group. Notably, the Smad2/3 protein expression was significantly higher in the non-MAFLD group compared to the control group (P < 0.05). On the other hand, the P-smad2/3 protein expression was significantly elevated in the MAFLD group compared to the control group (P < 0.001).
CONCLUSIONS
CONCLUSIONS
TGF-β signaling pathway in WBCs of patients with fatty liver are affected by a complex signaling pathway. However, metabolic factors most probably affect TGF-β1 gene expression and its downstream signaling proteins more than TGF-β3.
Identifiants
pubmed: 39352573
doi: 10.1007/s11033-024-09973-w
pii: 10.1007/s11033-024-09973-w
doi:
Substances chimiques
Smad2 Protein
0
Smad3 Protein
0
SMAD2 protein, human
0
Connective Tissue Growth Factor
139568-91-5
Transforming Growth Factor beta1
0
SMAD3 protein, human
0
Transforming Growth Factor beta
0
Smad Proteins
0
CCN2 protein, human
0
Transforming Growth Factor beta3
0
TGFB1 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1031Subventions
Organisme : Hamadan University of Medical Sciences
ID : 1402112410277
Informations de copyright
© 2024. The Author(s), under exclusive licence to Springer Nature B.V.
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