Evidence map›Paper›PMID 27242268›Full record

ReviewFree radical biology & medicine2016

Redox biology and the interface between bioenergetics, autophagy and circadian control of metabolism.

Adam R Wende, Martin E Young, John Chatham, Jianhua Zhang, Namakkal S Rajasekaran, Victor M Darley-Usmar

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

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  5. Circadian biology of cardiac aging.Journal of molecular and cellular cardiology · 2025
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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

6 authors at 2 institutions in 1 country.

Adam R WendeDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Martin E YoungDepartment of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
John ChathamDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Jianhua ZhangDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Namakkal S RajasekaranDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Victor M Darley-UsmarDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; UAB Mitochondrial Medicine Laboratory, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: vdarleyusmar@uabmc.edu.
University of Alabama at Birmingham · USMitochondria Research and Medicine Society · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Sex hormones and arthritis in a long lived animal modelP30AG050886 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Jianhua Zhang · 2015 to 2026
$11.3M
Reductive Stress Induces Proteotoxic Cardiac DiseaseR01HL118067 · NHLBI · UNIVERSITY OF UTAH · PI NAMAKKAL SOORAPPAN, RAJASEKARAN · 2013 to 2021
$4.5M
Disruption of the Clock O-GlcNAc axis in diabetic cardiomyopathyR01HL122975 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C, YOUNG, MARTIN E · 2015 to 2018
$1.6M
Protein O-GlcNAcylation and the regulation of cardiac functionR01HL101192 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2010 to 2014
$1.5M
Circadian Regulation of Myocardial Insulin SignalingR01HL123574 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2014 to 2017
$1.5M
Mechanisms of glucose mediated cardiac mitochondrial dysfunctionR00HL111322 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2013 to 2015
$870k
Antioxidant Defense Mechanisms: Nrf2/Keap1 Signaling in Aging HeartR03AG042860 · NIA · UNIVERSITY OF UTAH · PI NAMAKKAL SOORAPPAN, RAJASEKARAN · 2012 to 2013
$145k
NHLBI NIH HHS R00 HL111322NHLBI NIH HHS R01 HL101192NHLBI NIH HHS R01 HL118067NHLBI NIH HHS R01 HL122975NHLBI NIH HHS R01 HL123574NIA NIH HHS P30 AG050886NIA NIH HHS R03 AG042860NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Understanding molecular mechanisms that underlie the recent emergence of metabolic diseases such as diabetes and heart failure has revealed the need for a multi-disciplinary research integrating the key metabolic pathways which change the susceptibility to environmental or pathologic stress. At the physiological level these include the circadian control of metabolism which aligns metabolism with temporal demand. The mitochondria play an important role in integrating the redox signals and metabolic flux in response to the changing activities associated with chronobiology, exercise and diet. At the molecular level this involves dynamic post-translational modifications regulating transcription, metabolism and autophagy. In this review we will discuss different examples of mechanisms which link these processes together. An important pathway capable of linking signaling to metabolism is the post-translational modification of proteins by O-linked N-acetylglucosamine (O-GlcNAc). This is a nutrient regulated protein modification that plays an important role in impaired cellular stress responses. Circadian clocks have also emerged as critical regulators of numerous cardiometabolic processes, including glucose/lipid homeostasis, hormone secretion, redox status and cardiovascular function. Central to these pathways are the response of autophagy, bioenergetics to oxidative stress, regulated by Keap1/Nrf2 and mechanisms of metabolic control. The extension of these ideas to the emerging concept of bioenergetic health will be discussed.

Indexed as

AutophagyCircadian ClocksEnergy MetabolismSignal TransductionAcetylglucosamineAnimalsHumansKelch-Like ECH-Associated Protein 1MitochondriaOxidation-ReductionOxidative StressProtein Processing, Post-TranslationalAcetylglucosamineKelch-Like ECH-Associated Protein 1ChronobiologyKeap1Metabolic shiftNrf2Oxidative stressReserve capacity

Identifiers

PMID27242268
PMCPMC5124549
OpenAlexW2398580003

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.