Evidence map›Paper›PMID 38378001›Full record

ArticleCell metabolism2024

IgG is an aging factor that drives adipose tissue fibrosis and metabolic decline.

Lexiang Yu, Qianfen Wan, Qiongming Liu, Yong Fan, Qiuzhong Zhou, Alicja A Skowronski, Summer Wang, Zhengping Shao, Chen-Yu Liao, Lei Ding and 7 more

Open access · greenAbstract read
In one paragraph

Article in Cell metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
30.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  7. AAV-mediated FGF21 gene therapy promotes health span extension by whole-body tissue-specific adaptations.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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24 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 6 institutions in 3 countries.

Lexiang YuNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Qianfen WanNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Qiongming LiuNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Yong FanNaomi Berrie Diabetes Center, Department of Medicine, Columbia University, New York, NY 10032, USA.
Qiuzhong ZhouCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
Alicja A SkowronskiNaomi Berrie Diabetes Center, Department of Pediatrics, Columbia University, New York, NY 10032, USA.
Summer WangInstitute for Cancer Genetics, Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.
Zhengping ShaoInstitute for Cancer Genetics, Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.
Chen-Yu LiaoBuck Institute for Research on Aging, Novato, CA 94945, USA.
Lei DingDepartment of Rehabilitation and Regenerative Medicine, Department of Microbiology and Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Brian K KennedyBuck Institute for Research on Aging, Novato, CA 94945, USA; Healthy Longevity Translational Research Programme, Departments of Biochemistry and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Centre for Health Longevity, National University Health System, Singapore, Singapore.
Shan ZhaInstitute for Cancer Genetics, Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.
Jianwen QueDepartment of Medicine, Columbia University, New York, NY 10032, USA.
Charles A LeDucNaomi Berrie Diabetes Center, Department of Pediatrics, Columbia University, New York, NY 10032, USA.
Lei SunCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
Liheng WangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; Department of Medicine, Division of Endocrinology, Diabetes, Obesity, and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: lihengwang@hsc.pku.edu.cn.
Li QiangDepartment of Pharmacology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Naomi Berrie Diabetes Center, Department of Medicine, Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA. Electronic address: qiang@hsc.pku.edu.cn.
Columbia University · USCancer Genetics (United States) · USBuck Institute for Research on Aging · USDuke-NUS Medical School · SGPeking University · CNColumbia University Irving Medical Center · US

Funding

Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Anthony W Ferrante · 2003 to 2026
$36.7M
PPARgamma Deacetylation in the Restoration of Metabolic HomeostasisR01DK112943 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI QIANG, LI · 2018 to 2022
$2.4M
IgG and Adipose Pathological RemodelingR01DK134471 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Anthony W Ferrante · 2023 to 2026
$1.9M
NIDDK NIH HHS P30 DK063608NIDDK NIH HHS R01 DK112943NIDDK NIH HHS R01 DK134471
6 · The paper itself

Abstract

Aging 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.

Indexed as

Adipose TissueAgingAdipose Tissue, WhiteAnimalsFibrosisImmunoglobulin GMiceMice, KnockoutImmunoglobulin Gadipose tissueagingfibrosisIgGmetabolic dysfunction

Identifiers

PMID38378001
PMCPMC11070064
OpenAlexW4391934156

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.