Evidence map›Paper›PMID 28778689›Full record

ArticleLife sciences2017

Autophagosome formation is required for cardioprotection by chloramphenicol.

Zoltán Giricz, Zoltán V Varga, Gábor Koncsos, Csilla Terézia Nagy, Anikó Görbe, Robert M Mentzer, Roberta A Gottlieb, Péter Ferdinandy

Abstract read
In one paragraph

Article in Life sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
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  4. Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023
    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

8 authors at 2 institutions in 2 countries.

Zoltán GiriczCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary. Electronic address: giricz.zoltan@med.semmelweis-univ.hu.
Zoltán V VargaCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Gábor KoncsosCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Csilla Terézia NagyCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Anikó GörbeCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
Robert M MentzerHeart Institute, Cedars-Sinai Medical Center, CA, USA.
Roberta A GottliebHeart Institute, Cedars-Sinai Medical Center, CA, USA.
Péter FerdinandyCardiovascular and Metabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; Pharmahungary Group, Szeged, Hungary.
Semmelweis University · HUCedars-Sinai Medical Center · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
Protein Chemistry and ProteomicsP01HL112730 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI VAN EYK, JENNIFER E · 2013 to 2017
$12.0M
NHLBI NIH HHS P01 HL085577NHLBI NIH HHS P01 HL112730
6 · The paper itself

Abstract

aimsChloramphenicol (CAP), a broad spectrum antibiotic, was shown to protect the heart against ischemia/reperfusion (I/R) injury. CAP also induces autophagy, however, it is not known whether CAP-induced cardioprotection is mediated by autophagy. Therefore, here we aimed to assess whether activation of autophagy is required for the infarct size limiting effect of CAP and to identify which component of CAP-induced autophagy contributes to cardioprotection against I/R injury. MAIN

methodsHearts of Sprague-Dawley rats were perfused in Langendorff mode with Krebs-Henseleit solution containing either vehicle (CON), 300μM CAP (CAP), CAP and an inhibitor of autophagosome-lysosome fusion chloroquine (CAP+CQ), or an inhibitor of autophagosome formation, the functional null mutant TAT-HA-Atg5 KEY

findingsCAP treatment induced autophagy, increased phosphorylation of Erk1/2 in the myocardium and significantly reduced infarct size and CK release. Autophagy inhibitor TAT-HA-Atg5

conclusionThis is the first demonstration that autophagosome formation but not autophagosomal clearance is required for CAP-induced cardioprotection. SIGNIFICANCE: Inducing autophagy sequestration might yield novel therapeutic options against acute ischemia/reperfusion injury.

Indexed as

AnimalsAutophagosomesAutophagyCardiotonic AgentsChloramphenicolCoronary CirculationIn Vitro TechniquesMAP Kinase Signaling SystemMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacPilot ProjectsRats, Sprague-DawleyCardiotonic AgentsChloramphenicolAutophagyCardioprotectionChloramphenicol

Identifiers

PMID28778689
PMCPMC6242268
OpenAlexW2740553011

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.