Low plasma growth/differentiation factor 1 levels are associated with liver fibrosis in patients with stable angina

Background Growth differentiation factor 1 (GDF1) is a member of the transforming growth factor‐β (TGF‐β) superfamily and a protective mediator against the development of post‐infarction cardiac remodeling by negatively regulating MEK‐ERK1/2 and Smad signaling pathways in the heart. The TGF‐β/SMAD p...

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Published in:Journal of clinical laboratory analysis 2022-11, Vol.36 (11), p.e24745-n/a
Main Authors: Hung, Wei‐Chin, Tang, Wei‐Hua, Yu, Teng‐Hung, Wu, Cheng‐Ching, Wang, Chao‐Ping, Lu, Yung‐Chuan, Wei, Ching‐Ting, Chung, Fu‐Mei, Lee, Yau‐Jiunn, Hsu, Chia‐Chang
Format: Article
Language:English
Subjects:
Age
Alanine transaminase
Alcohol
Angina
Angina pectoris
Aspartate aminotransferase
Automation
Blood platelets
Blood pressure
Body mass index
Cardiovascular disease
Cholesterol
Creatinine
Diabetes
Fasting
Fatty liver
Fibrosis
Growth differentiation factor 1
Heart attacks
Hemoglobin
High density lipoprotein
Hypertension
Infarction
Liver diseases
liver fibrosis
Medical imaging
MEK‐ERK1/2
Metabolism
Patients
Plasma
Regression analysis
Signal transduction
Smad protein
Smad signaling
stable angina
Trends
Triglycerides
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Summary:Background Growth differentiation factor 1 (GDF1) is a member of the transforming growth factor‐β (TGF‐β) superfamily and a protective mediator against the development of post‐infarction cardiac remodeling by negatively regulating MEK‐ERK1/2 and Smad signaling pathways in the heart. The TGF‐β/SMAD pathway has been shown to play a key role in the development of hepatic fibrosis. In addition, fatty liver disease has been associated with reduced MEK/ERK1/2 signaling. However, no previous study has investigated the association between GDF1 and liver fibrosis. Therefore, the aim of this study was to investigate the association between plasma GDF1 and liver fibrosis in patients with stable angina. Methods We included 327 consecutive patients with stable angina. ELISA was used to measure circulating levels of GDF1, and the fibrosis‐4 index was used to assess liver fibrosis. Results The advanced liver fibrosis group had lower median plasma GDF1 levels than those with minimal liver fibrosis. There was a significant negative association between GDF1 plasma level and fibrosis‐4 index (r = −0.135, p = 0.019). A lower concentration of GDF1 was significantly and independently associated with an increased risk of liver fibrosis when concentration was analyzed as a continuous variable and by tertile. In addition, fibrosis‐4 index, aspartate aminotransferase (AST)‐to‐platelet ratio index, and AST/alanine aminotransferase ratio were significantly associated with GDF1 concentration. Conclusions Our results indicated an association between low plasma GDF1 and liver fibrosis in the enrolled patients. Further investigations into the role of plasma GDF1 in the pathogenesis of liver fibrosis are warranted. Classification of subjects into tertiles according to growth/differentiation factor 1 (GDF1) concentration revealed that the fibrosis‐4 index (A), aspartate aminotransferase to platelet ratio index (B), and aspartate aminotransferase/ alanine aminotransferase ratio (C) were significantly associated with GDF1 concentration (p for trend 
ISSN:0887-8013
1098-2825
DOI:10.1002/jcla.24745