First-pass extracted concept

THBS1

Candidate: concept label1 source documents4 linked claims

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Aliases

Thrombospondin-1

Evidence Snippets

THBS1 is a key pro-fibrotic factor in IUA, modulating the PI3K/AKT pathway.

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2026MEDDOI PubMed

1 evidence snippet 4 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1comparative therapeutic effectsupports2026Source 1DOI PubMed

DMSC treatment shows a more pronounced anti-fibrotic effect than THBS1 silencing in vitro and may involve THBS1 regulation.

Quoted textsource-backed

DMSC treatment showed a more pronounced anti-fibrotic effect, suggesting that DMSC-mediated repair involves THBS1 regulation.

Claim 2mechanistic rolesupports2026Source 1DOI PubMed

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 3perturbation effectsupports2026Source 1DOI PubMed

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 4therapeutic effectsupports2026Source 1DOI PubMed

In vivo, both THBS1 knockdown and DMSC administration alleviate intrauterine fibrosis, reduce inflammation, and enhance angiogenesis.

Quoted textsource-backed

In vivo, both THBS1 knockdown and DMSC administration alleviated intrauterine fibrosis, reduced inflammation, and enhanced angiogenesis.