Evidence map›Paper›PMID 22076133›Full record

ArticlePloS one2011

Age-associated disruption of molecular clock expression in skeletal muscle of the spontaneously hypertensive rat.

Mitsunori Miyazaki, Elizabeth Schroder, Stephanie E Edelmann, Michael E Hughes, Karl Kornacker, C William Balke, Karyn A Esser

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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

7 authors at 4 institutions in 1 country.

Mitsunori MiyazakiDepartment of Physiology, Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, United States of America.
Elizabeth Schroder
Stephanie E Edelmann
Michael E Hughes
Karl Kornacker
C William Balke
Karyn A Esser
University of Kentucky · USSouthern California Clinical and Translational Science Institute · USThe Ohio State University · USYale University · US

Funding

Circadian rhythms and skeletal muscleR01AR055246 · NIAMS · UNIVERSITY OF KENTUCKY · PI ESSER, KARYN A · 2008 to 2012
$1.6M
Clock genes, environmental challenges and cardiopulmonary diseaseRC1ES018636 · NIEHS · UNIVERSITY OF KENTUCKY · PI ANDRADE, FRANCISCO H, ESSER, KARYN A · 2009 to 2010
$996k
NIAMS NIH HHS R01 AR055246NIAMS NIH HHS R01AR055246NIEHS NIH HHS RC1 ES018636NIEHS NIH HHS RC1ES018636
6 · The paper itself

Abstract

It is well known that spontaneously hypertensive rats (SHR) develop muscle pathologies with hypertension and heart failure, though the mechanism remains poorly understood. Woon et al. (2007) linked the circadian clock gene Bmal1 to hypertension and metabolic dysfunction in the SHR. Building on these findings, we compared the expression pattern of several core-clock genes in the gastrocnemius muscle of aged SHR (80 weeks; overt heart failure) compared to aged-matched control WKY strain. Heart failure was associated with marked effects on the expression of Bmal1, Clock and Rora in addition to several non-circadian genes important in regulating skeletal muscle phenotype including Mck, Ttn and Mef2c. We next performed circadian time-course collections at a young age (8 weeks; pre-hypertensive) and adult age (22 weeks; hypertensive) to determine if clock gene expression was disrupted in gastrocnemius, heart and liver tissues prior to or after the rats became hypertensive. We found that hypertensive/hypertrophic SHR showed a dampening of peak Bmal1 and Rev-erb expression in the liver, and the clock-controlled gene Pgc1α in the gastrocnemius. In addition, the core-clock gene Clock and the muscle-specific, clock-controlled gene Myod1, no longer maintained a circadian pattern of expression in gastrocnemius from the hypertensive SHR. These findings provide a framework to suggest a mechanism whereby chronic heart failure leads to skeletal muscle pathologies; prolonged dysregulation of the molecular clock in skeletal muscle results in altered Clock, Pgc1α and Myod1 expression which in turn leads to the mis-regulation of target genes important for mechanical and metabolic function of skeletal muscle.

Indexed as

Gene Expression Regulation, DevelopmentalAge FactorsAnimalsBlotting, WesternCircadian ClocksCLOCK ProteinsDNA-Binding ProteinsHeartHypertensionLiverMaleMuscle, SkeletalMyoD ProteinNuclear Receptor Subfamily 1, Group D, Member 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsCLOCK ProteinsDBP protein, ratDNA-Binding ProteinsMyoD1 myogenic differentiation proteinMyoD ProteinNuclear Receptor Subfamily 1, Group D, Member 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratRNA-Binding ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID22076133
PMCPMC3208587
OpenAlexW2112265284

What OpenQuestion holds

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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.