IgG accumulates in adipose tissue during aging and is reduced by caloric restriction
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Yu, L., Wan, Q., & Liu, Q. (2024). IgG is an aging factor that drives adipose tissue fibrosis and metabolic decline. Cell Metabolism, 36(4), 793–507. Added by: Dr. Enrique Feoli (04/08/2025, 00:07) Last edited by: Dr. Enrique Feoli (04/08/2025, 00:10) |
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| Resource type: Journal Article ID no. (ISBN etc.): 1550-4131 BibTeX citation key: Yu2024 View all bibliographic details  |
Categories: BioAcyl Corp Keywords: adipose tissue, Aging, Fibrosis, IgG, metabolic dysfunction Creators: Liu, Wan, Yu Publisher: Cell Press Collection: Cell Metabolism |
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| Abstract |
SummaryAging is underpinned by pronounced metabolic decline; however, the drivers remain obscure. Here, we report that IgG accumulates during aging, particularly in white adipose tissue (WAT), to impair adipose tissue function and metabolic health. Caloric restriction (CR) decreases IgG accumulation in WAT, whereas replenishing IgG counteracts CR’s metabolic benefits. IgG activates macrophages via Ras signaling and consequently induces fibrosis in WAT through the TGF-β/SMAD pathway. Consistently, B cell null mice are protected from aging-associated WAT fibrosis, inflammation, and insulin resistance, unless exposed to IgG. Conditional ablation of the IgG recycling receptor, neonatal Fc receptor (FcRn), in macrophages prevents IgG accumulation in aging, resulting in prolonged healthspan and lifespan. Further, targeting FcRn by antisense oligonucleotide restores WAT integrity and metabolic health in aged mice. These findings pinpoint IgG as a hidden culprit in aging and enlighten a novel strategy to rejuvenate metabolic health.
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