“
TL;DR
It describes how TRIM proteins, as E3 ubiquitin ligases, modulate signaling pathways such as MAPK, NF-κB, and TGF-β, which are linked to insulin resistance, inflammation, fibrosis, and ferroptosis in MAFLD.
Frontiers in Endocrinology · 5 authors, 2 centres
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
It describes how TRIM proteins, as E3 ubiquitin ligases, modulate signaling pathways such as MAPK, NF-κB, and TGF-β, which are linked to insulin resistance, inflammation, fibrosis, and ferroptosis in MAFLD.
It describes how TRIM proteins, as E3 ubiquitin ligases, modulate signaling pathways such as MAPK, NF-κB, and TGF-β, which are linked to insulin resistance, inflammation, fibrosis, and ferroptosis in MAFLD. The review highlights specific TRIM members, noting that TRIM38 inhibits steatosis and fibrosis in vitro and in mice, while TRIM59 promotes steatosis and ferroptosis.