Evidence map›Paper›PMID 31402172›Full record

ArticleCell2019

GDF15 Is an Inflammation-Induced Central Mediator of Tissue Tolerance.

Harding H Luan, Andrew Wang, Brandon K Hilliard, Fernando Carvalho, Connor E Rosen, Amy M Ahasic, Erica L Herzog, Insoo Kang, Margaret A Pisani, Shuang Yu and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 341 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
341citing papers in PubMed, 4 pooled it
43.8field-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

341 citing papers in PubMed, 4 syntheses or guidelines pooled it, 487 citations in OpenAlex.

  1. Pooled it
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  12. Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026
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281 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Harding H LuanDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Andrew WangDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Medicine (Rheumatology), Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: andrew.wang@yale.edu.
Brandon K HilliardDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Medicine (Rheumatology), Yale University School of Medicine, New Haven, CT 06520, USA.
Fernando CarvalhoDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Connor E RosenDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Amy M AhasicDepartment of Medicine (Pulmonary, Critical Care and Sleep), Yale University School of Medicine, New Haven, CT 06520, USA.
Erica L HerzogDepartment of Medicine (Pulmonary, Critical Care and Sleep), Yale University School of Medicine, New Haven, CT 06520, USA.
Insoo KangDepartment of Medicine (Rheumatology), Yale University School of Medicine, New Haven, CT 06520, USA.
Margaret A PisaniDepartment of Medicine (Pulmonary, Critical Care and Sleep), Yale University School of Medicine, New Haven, CT 06520, USA.
Shuang YuDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Cuiling ZhangDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Medicine (Rheumatology), Yale University School of Medicine, New Haven, CT 06520, USA.
Aaron M RingDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Lawrence H YoungDepartment of Medicine (Cardiology), Yale University School of Medicine, New Haven, CT 06520, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA.
Ruslan MedzhitovDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: ruslan.medzhitov@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI WAJAHAT Zafar MEHAL · 1986 to 2026
$31.1M
Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 2008 to 2022
$16.8M
PREDOCTORAL TRAINING PROGRAM IN MICROBIAL PATHOGENESIST32AI007640 · NIAID · YALE UNIVERSITY · PI GOODMAN, ANDREW L · 2000 to 2022
$4.3M
Novel Immunologic Effects of Semaphorin 7a in IPFR01HL109233 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2011 to 2019
$3.7M
Role of GDF15 in the Regulation of Host Tolerance to InflammationR01AI144152 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2019 to 2023
$2.1M
Neuroimmune Molecules in Scleroderma Lung FibrosisR01HL125850 · NHLBI · YALE UNIVERSITY · PI HERZOG, ERICA L · 2016 to 2019
$1.7M
Regulation of Metabolic Programs for Host Tolerance to InflammationK08AI128745 · NIAID · YALE UNIVERSITY · PI WANG, ANDREW · 2017 to 2021
$784k
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863NHLBI NIH HHS R01 HL109233NHLBI NIH HHS R01 HL125850NIAID NIH HHS K08 AI128745NIAID NIH HHS R01 AI144152NIAID NIH HHS T32 AI007640NIDDK NIH HHS P30 DK034989NIDDK NIH HHS P30 DK079310
6 · The paper itself

Abstract

Growth and differentiation factor 15 (GDF15) is an inflammation-associated hormone with poorly defined biology. Here, we investigated the role of GDF15 in bacterial and viral infections. We found that inflammation induced GDF15, and that GDF15 was necessary for surviving both bacterial and viral infections, as well as sepsis. The protective effects of GDF15 were largely independent of pathogen control or the magnitude of inflammatory response, suggesting a role in disease tolerance. Indeed, we found that GDF15 was required for hepatic sympathetic outflow and triglyceride metabolism. Failure to defend the lower limit of plasma triglyceride levels was associated with impaired cardiac function and maintenance of body temperature, effects that could be rescued by exogenous administration of lipids. Together, we show that GDF15 coordinates tolerance to inflammatory damage through regulation of triglyceride metabolism.

Indexed as

AnimalsAntibodiesDisease Models, AnimalGrowth Differentiation Factor 15HeartHumansLipid MetabolismLipopolysaccharidesLiverMiceMice, Inbred C57BLNorepinephrineOrthomyxoviridaePoly I-CRecombinant ProteinsSepsisAntibodiesGrowth Differentiation Factor 15LipopolysaccharidesNorepinephrinePoly I-CRecombinant ProteinsTriglyceridesTroponin ITumor Necrosis Factor-alphaadrenergic signalingcardioprotectionGDF15inflammationmetabolismneuroimmunologysepsistolerancetriglyceride

Identifiers

PMID31402172
PMCPMC6863354
OpenAlexW2967524380

What OpenQuestion holds

Textmetadata
LicenceTDM
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.