First-pass extracted concept

PI3K/AKT signaling pathway

Candidate: concept label2 source documents3 linked claims
Live refresh every 5sNext refresh in 5s

Evidence Snippets

Pathway analysis suggested that THBS1 promotes fibrosis via the PI3K/AKT pathway.
Evidence 1Source 1DOIPubMedprovenance
These signaling pathways include... tyrosine phosphatidylinositol 3-kinase (PI3K)/AKT...
Evidence 2Source 2DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1mechanistic rolesupports2026Source 1DOIPubMed

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.
Claim 2perturbation effectsupports2026Source 1DOIPubMed

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.
Claim 3review scope summarysupports2023Source 2DOIPubMed

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.