Evidence map›Paper›PMID 26997632›Full record

ArticlePhysiological reports2016

Immunomodulatory roles of CTRP3 in endotoxemia and metabolic stress.

Pia S Petersen, Risa M Wolf, Xia Lei, Jonathan M Peterson, G William Wong

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  4. Decreased EpicardialInternational journal of molecular sciences · 2022
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  12. Late-onset renal hypertrophy and dysfunction in mice lacking CTRP1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. Review
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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

5 authors at 2 institutions in 1 country.

Pia S PetersenDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland Center for Metabolism and Obesity Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Risa M WolfDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland Center for Metabolism and Obesity Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Xia LeiDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland Center for Metabolism and Obesity Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jonathan M PetersonDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland Center for Metabolism and Obesity Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
G William WongDepartment of Physiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland Center for Metabolism and Obesity Research, The Johns Hopkins University School of Medicine, Baltimore, Maryland gwwong@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

CTRP and Metabolic ControlR01DK084171 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI Guang William Wong · 2010 to 2026
$8.0M
NIDDK NIH HHS R01 DK084171NIDDK NIH HHS R01DK084171
6 · The paper itself

Abstract

C1q/TNF-related protein 3 (CTRP3) is a secreted hormone that modulates hepatic glucose and lipid metabolism. Its circulating levels are reduced in human and rodent models of obesity, a metabolic state accompanied by chronic low-grade inflammation. Recent studies have demonstrated an anti-inflammatory role for recombinant CTRP3 in attenuating LPS-induced systemic inflammation, and its deficiency markedly exacerbates inflammation in a mouse model of rheumatoid arthritis. We used genetic mouse models to explore the immunomodulatory function of CTRP3 in response to acute (LPS challenge) and chronic (high-fat diet) inflammatory stimuli. In a sublethal dose of LPS challenge, neither CTRP3 deficiency nor its overexpression in transgenic mice had an impact on IL-1β, IL-6, TNF-α, or MIP-2 induction at the serum protein or mRNA levels, contrary to previous findings based on recombinant CTRP3 administration. In a metabolic context, we measured 71 serum cytokine levels in wild-type and CTRP3 transgenic mice fed a high-fat diet or a matched control low-fat diet. On a low-fat diet, CTRP3 transgenic mice had elevated circulating levels of multiple chemokines (CCL11, CXCL9, CXCL10, CCL17, CX3CL1, CCL22 and sCD30). However, when obesity was induced with a high-fat diet, CTRP3 transgenic mice had lower circulating levels of IL-5, TNF-α, sVEGF2, and sVEGFR3, and a higher level of soluble gp130. Contingent upon the metabolic state, CTRP3 overexpression altered chemokine levels in lean mice, and attenuated systemic inflammation in the setting of obesity and insulin resistance. These results highlight a context-dependent immunomodulatory role for CTRP3.

Indexed as

AdipokinesAnimalsDiet, Fat-RestrictedDiet, High-FatEndotoxemiaImmunologic FactorsInflammation MediatorsLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicObesityStress, PhysiologicalAdipokinesCORS26 protein, mouseImmunologic FactorsInflammation MediatorsCTRP3cytokinesinflammationLPSobesity

Identifiers

PMID26997632
PMCPMC4823594
OpenAlexW2309763940

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.