Evidence map›Paper›PMID 26519034›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

The cardioprotective compound cloxyquin uncouples mitochondria and induces autophagy.

Jimmy Zhang, Sergiy M Nadtochiy, William R Urciuoli, Paul S Brookes

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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  10. 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

4 authors at 1 institution in 1 country.

Jimmy ZhangDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York;ORCID http://orcid.org/0000-0001-7869-8005
Sergiy M NadtochiyDepartment of Anesthesiology, University of Rochester Medical Center, Rochester, New York.
William R UrciuoliDepartment of Anesthesiology, University of Rochester Medical Center, Rochester, New York.
Paul S BrookesDepartment of Anesthesiology, University of Rochester Medical Center, Rochester, New York paul_brookes@urmc.rochester.edu.
University of Rochester Medical Center · US

Funding

University of Rochester Mentoring Environment: Nurturing Training Opportunities in Research (UR-MENTOR)T32GM007356 · NIGMS · UNIVERSITY OF ROCHESTER · PI O'BANION, M. KERRY · 1985 to 2023
$15.1M
SIRT1, Nitro-Lipids and CardioprotectionR01HL071158 · NHLBI · UNIVERSITY OF ROCHESTER · PI BROOKES, PAUL S · 2003 to 2025
$7.7M
NHLBI NIH HHS R01 HL-071158NHLBI NIH HHS R01 HL071158NIGMS NIH HHS T32 GM-007356NIGMS NIH HHS T32 GM007356
6 · The paper itself

Abstract

Mitochondrial quality control mechanisms have been implicated in protection against cardiac ischemia-reperfusion (IR) injury. Previously, cloxyquin (5-chloroquinolin-8-ol) was identified via phenotypic screening as a cardioprotective compound. Herein, cloxyquin was identified as a mitochondrial uncoupler in both isolated heart mitochondria and adult cardiomyocytes. Additionally, cardiomyocytes isolated from transgenic mice expressing green fluorescent protein-tagged microtubule-associated protein light chain 3 showed increased autophagosome formation with cloxyquin treatment. The autophagy inhibitor chloroquine abolished cloxyquin-induced cardioprotection in both cellular and perfused heart (Langendorff) models of IR injury. Finally, in an in vivo murine left anterior descending coronary artery occlusion model of IR injury, cloxyquin significantly reduced infarct size from 31.4 ± 3.4% to 16.1 ± 2.2%. In conclusion, the cardioprotective compound cloxyquin simultaneously uncoupled mitochondria and induced autophagy. Importantly, autophagy appears to be required for cloxyquin-induced cardioprotection.

Indexed as

AnimalsAutophagyChloroquineChloroquinolinolsDose-Response Relationship, DrugGreen Fluorescent ProteinsIsolated Heart PreparationMaleMice, Inbred C57BLMice, TransgenicMicrotubule-Associated ProteinsMitochondria, HeartMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacProtective AgentsChloroquineChloroquinolinolscloxyquinGreen Fluorescent ProteinsMicrotubule-Associated ProteinsProtective AgentsRecombinant Fusion ProteinsUncoupling Agents8-hydroxyquinolineheartischemiamitophagyuncoupling

Identifiers

PMID26519034
PMCPMC4796459
OpenAlexW2269587458

What OpenQuestion holds

Textmetadata
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.