PebbleAtlas
PEBBLE / ATLAS
Open research access
PRECLINICAL PUBLICATION · 2019

CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization.

Mouse / Chemical/toxin

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 31481754 ↗2019Reported benefit

CCL5 deficiency promotes liver repair by improving inflammation resolution and liver regeneration through M2 macrophage polarization.

MouseChemical/toxin

Model: Acetaminophen-induced acute liver injury

CCL5 deficiency did not alter the early phase but promoted late-phase liver repair through inflammation resolution and regeneration with more hepatic M2 macrophages; CCL5 blockade with a neutralising antibody or Met-CCL5 alleviated liver injury and improved survival.

Extraction: extract · Supplied extraction confidence: 0.6. Machine-extracted fields require source verification.