Pathway analysis suggested that THBS1 promotes fibrosis via the PI3K/AKT pathway.
First-pass extracted concept
PI3K/AKT signaling pathway
Candidate: concept label2 source documents3 linked claims
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Supporting Sources
Linked Claims
THBS1 is upregulated in intrauterine adhesion tissues and is implicated as a pro-fibrotic factor acting through the PI3K/AKT pathway.
Quoted textsource-backed
Transcriptomic profiling identified significant upregulation of THBS1 in IUA tissues. Pathway analysis suggested that THBS1 promotes fibrosis via the PI3K/AKT pathway.
THBS1 silencing reduces fibrotic markers and inhibits PI3K/AKT pathway activation in vitro.
Quoted textsource-backed
THBS1 silencing reduced fibrotic markers and inhibited PI3K/AKT pathway activation in vitro.
The review summarizes that several natural compounds modify multiple inflammation-associated signaling pathways, including NF-κB, AP-1, PTKs, MAPKs, Nrf2, PI3K/AKT, and the ubiquitin-proteasome system.
Quoted textsource-backed
Through current study, an attempt is made to outline and highlight a wide variety of inflammation-associated signaling pathways that have been modified by several natural compounds. These signaling pathways include nuclear factor-kappa B (NF-κB), activator protein (AP)-1, protein tyrosine kinases (PTKs), mitogen-activated protein kinases (MAPKs), nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factors, tyrosine phosphatidylinositol 3-kinase (PI3K)/AKT, and the ubiquitin-proteasome system.