Researchers have uncovered how metabolic reprogramming contributes to renal fibrosis in IgG4-related disease (IgG4-RD), a systemic immune-mediated disorder. The review, published in a leading journal, details how immune cell metabolism shifts—such as mitochondrial dysfunction and glycolytic activation—drive fibrotic processes through pathways like TGF-β/SMAD3 and AMPK-PPARγ. The study also explores the role of ABC transporters in drug resistance and proposes metabolomics and multi-omics integration as tools for early diagnosis and personalized treatment. These findings open new avenues for targeting metabolic pathways to reverse fibrosis in IgG4-RD.
LabMed Discovery
News article
Metabolic Reprogramming Mechanism of Renal Fibrosis in IgG4-Related Disease: From Immune Dysregulation to Imbalance of Energy Homeostasis
5-Sep-2025