First-pass extracted concept

fibrotic macrophage

Candidate: concept label1 source documents4 linked claims
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Aliases

Fib-Mac

Extracted Explainers

What the tool is doing

Fib-Mac is the paper's label for a profibrotic macrophage state. The abstract links this state to transcriptional and metabolic reprogramming and to worsened lung fibrosis.

Source 1DOIPubMed

What problem it solves

It gives a compact label for the pathogenic macrophage polarization state studied in this fibrosis context.

Source 1DOIPubMed

What it does not solve

The abstract alone does not specify the full molecular definition or how Fib-Mac maps to other published profibrotic macrophage labels.

Source 1DOIPubMed

Evidence Snippets

Here, we identify lysine-specific demethylase 7 A (KDM7A) as an epigenetic suppressor of a profibrotic macrophage (Fib-Mac).
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1disease model phenotypesupports2026Source 1DOIPubMed

Kdm7a-knockout mice show exacerbated bleomycin-induced lung fibrosis with expansion of fibrotic macrophage populations.

Quoted textsource-backed
Kdm7a-knockout mice exhibit exacerbated bleomycin-induced lung fibrosis with the expansion of Fib-Mac populations.
Claim 2mechanismsupports2026Source 1DOIPubMed

TLR8 suppresses fibrotic macrophage polarization and its expression is regulated by KDM7A via H3K27me2 at its enhancer.

Quoted textsource-backed
Mechanistically, we identify toll-like receptor 8 (TLR8) as a suppressor of Fib-Mac polarization whose expression is regulated by KDM7A via the repressive mark H3K27me2 at its enhancer.
Claim 3mechanistic rolesupports2026Source 1DOIPubMed

KDM7A acts as an epigenetic suppressor of profibrotic macrophage polarization.

Quoted textsource-backed
Here, we identify lysine-specific demethylase 7 A (KDM7A) as an epigenetic suppressor of a profibrotic macrophage (Fib-Mac).
Claim 4perturbation effectsupports2026Source 1DOIPubMed

Loss of Kdm7a drives transcriptional and metabolic reprogramming toward fibrotic macrophage states.

Quoted textsource-backed
we show that Kdm7a loss drives transcriptional and metabolic reprogramming toward Fib-Mac states.