2022
DOI: 10.1007/s12013-022-01079-z
|View full text |Cite
|
Sign up to set email alerts
|

Preventive Effect and Mechanism of Anthocyanins from Aronia Melanocarpa Elliot on Hepatic Fibrosis Through TGF-β/Smad Signaling Pathway

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2

Citation Types

0
2
0

Year Published

2023
2023
2024
2024

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(2 citation statements)
references
References 24 publications
0
2
0
Order By: Relevance
“…1,2 However, when sustained injury and inflammation occur in the liver, the synthesis and degradation of extracellular matrix (ECM) rich in type I and III collagens are unbalanced, resulting in excessive increase and abnormal deposition of ECM. 3 Currently, the activation and proliferation of hepatic stellate cells (HSCs) is considered the central link of liver fibrosis. After activation, HSCs become myofibroblasts (MFBs), which synthesize substantial ECM to cause pathological precipitation of ECM in the liver, thereby leading to abnormal liver structure and function to ultimately develop liver fibrosis.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…1,2 However, when sustained injury and inflammation occur in the liver, the synthesis and degradation of extracellular matrix (ECM) rich in type I and III collagens are unbalanced, resulting in excessive increase and abnormal deposition of ECM. 3 Currently, the activation and proliferation of hepatic stellate cells (HSCs) is considered the central link of liver fibrosis. After activation, HSCs become myofibroblasts (MFBs), which synthesize substantial ECM to cause pathological precipitation of ECM in the liver, thereby leading to abnormal liver structure and function to ultimately develop liver fibrosis.…”
Section: Introductionmentioning
confidence: 99%
“…As an immunoresponse to liver injury and repair, liver fibrosis is a pathophysiological process in which scar tissue replaces damaged or necrotic one 1,2 . However, when sustained injury and inflammation occur in the liver, the synthesis and degradation of extracellular matrix (ECM) rich in type I and III collagens are unbalanced, resulting in excessive increase and abnormal deposition of ECM 3 . Currently, the activation and proliferation of hepatic stellate cells (HSCs) is considered the central link of liver fibrosis.…”
Section: Introductionmentioning
confidence: 99%