News Release

Metabolic reprogramming drives renal fibrosis in IgG4-related disease, revealing new therapeutic targets

Peer-Reviewed Publication

Shanghai Jiao Tong University Journal Center

Metabolic-Immune Crosstalk in IgG4-RD Renal Fibrosis

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Illustrates key mechanisms of metabolic reprogramming and immune cell interaction in renal fibrosis.

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Credit: Peng Lu,Maolin Liu,Lei Zhang,Jing-Jing Fan,Yan Sun.

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.


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