Evidence map›Paper›PMID 24366076›Full record

ArticleHypertension (Dallas, Tex. : 1979)2014

Macrophage migration inhibitory factor deletion exacerbates pressure overload-induced cardiac hypertrophy through mitigating autophagy.

Xihui Xu, Yinan Hua, Sreejayan Nair, Richard Bucala, Jun Ren

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The role of CD74 in cardiovascular disease.Frontiers in cardiovascular medicine · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Critical roles of macrophages in pressure overload-induced cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
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 1 institution in 1 country.

Xihui XuCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, 1000 E University Ave, Laramie, WY 82071. jren@uwyo.edu.
Yinan Hua
Sreejayan Nair
Richard Bucala
Jun Ren
University of Wyoming · US

Funding

Wyoming INBRE Phase 4- Equipment Supplement for x-ray diffractometer for Center for Advanced Scientific InstrumentationP20GM103432 · NIGMS · UNIVERSITY OF WYOMING · PI Robert Scott Seville · 2012 to 2026
$56.8M
Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI LIBERLES, DAVID A. · 2001 to 2011
$28.2M
MIF AND THE HOST RESPONSE TO INFECTIONR01AI042310 · NIAID · YALE UNIVERSITY · PI BUCALA, RICHARD J · 1998 to 2013
$4.3M
NCRR NIH HHS P20 RR016474NIAID NIH HHS R01 AI042310NIAID NIH HHS R01-AI042310NIGMS NIH HHS P20 GM103432
6 · The paper itself

Abstract

The proinflammatory cytokine macrophage migration inhibitory factor (MIF) has been shown to be cardioprotective under various pathological conditions. However, the underlying mechanisms still remain elusive. In this study, we revealed that MIF deficiency overtly exacerbated abdominal aorta constriction-induced cardiac hypertrophy and contractile anomalies. MIF deficiency interrupted myocardial autophagy in hypertrophied hearts. Rapamycin administration mitigated the exacerbated hypertrophic responses in MIF(-/-) mice. Using the phenylephrine-induced hypertrophy in vitro model in H9C2 myoblasts, we confirmed that MIF governed the activation of AMP-activated protein kinase-mammalian target of rapamycin-autophagy cascade. Confocal microscopic examination demonstrated that MIF depletion prevented phenylephrine-induced mitophagy in H9C2 myoblasts. Myocardial Parkin, an E3 ubiquitin ligase and a marker for mitophagy, was significantly upregulated after sustained pressure overload, the effect of which was prevented by MIF knockout. Furthermore, our data exhibited that levels of MIF, AMP-activated protein kinase activation, and autophagy were elevated concurrently in human failing hearts. These data indicate that endogenous MIF regulates the mammalian target of rapamycin signaling to activate autophagy to preserve cardiac geometry and protect against hypertrophic responses.

Indexed as

AutophagyAnimalsCardiomegalyDisease Models, AnimalHeart FailureHumansMacrophage Migration-Inhibitory FactorsMacrophagesMiceMicroscopy, ConfocalMyocardiumMyocytes, CardiacSignal TransductionMacrophage Migration-Inhibitory Factorsautophagycardiac hypertrophymacrophage migration inhibitory factormammalian target of rapamycinrapamycin

Identifiers

PMID24366076
PMCPMC3929844
OpenAlexW2136776017

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.