ABSTRACT
Toxocara canis
larvae migrate through the liver, where persistent tissue injury and immune‐mediated inflammation may promote granuloma formation and fibrosis. This review summarizes the histopathological and imaging features, cellular and molecular mechanisms, clinical assessment, and potential reversibility of
T. canis
‐induced liver fibrosis. Experimental evidence indicates that fibrosis is typically focal or multifocal and progresses from eosinophil‐rich inflammation and fibrocellular granulomas to collagen‐rich lesions, with a later predominance of collagen type I. Fibrogenesis involves hepatic stellate‐cell activation within a TGF‐β1‐, IL‐4/IL‐13‐, and alternatively activated macrophage‐associated microenvironment.
Toxocara
excretory‐secretory products, proteases, extracellular vesicles, and regulatory RNAs may further influence NF‐κB/MAPK, NOD1/2–RIP2, JAK/STAT, and IL‐33/ST2 signaling, although many proposed links remain indirect or unvalidated in the liver. Human evidence is limited mainly to imaging reports and small case series; the epidemiological contribution of toxocariasis to chronic fibrosis and cirrhosis therefore remains unknown. A preliminary murine study suggesting regression of chemically induced fibrosis after infection highlights the context‐dependent nature of parasite–host interactions but requires independent confirmation. Standardized human studies and clinically relevant experimental models are needed to define disease burden, validate biomarkers, and identify safe adjunctive antifibrotic strategies.