Evidence map›Paper›PMID 28467921›Full record

ReviewCell metabolism2017

Molecular Mechanisms Underlying Cardiac Adaptation to Exercise.

Rick B Vega, John P Konhilas, Daniel P Kelly, Leslie A Leinwand

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 3 pooled it
15.7field-weighted citation impact, top 1% 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

173 citing papers in PubMed, 3 syntheses or guidelines pooled it, 294 citations in OpenAlex.

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  18. Assessing the causal impact of leisure-time physical activity and screen time on lifespan: a Mendelian randomization study.European review of aging and physical activity : official journal of the European Group for Research into Elderly and Physical Activity · 2026
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113 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Rick B VegaCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, FL 32827, USA.
John P KonhilasDepartment of Physiology, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85724, USA.
Daniel P KellyCenter for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, FL 32827, USA.
Leslie A LeinwandMolecular, Cellular and Developmental Biology, BioFrontiers Institute, University of Colorado, Boulder, CO 80309, USA. Electronic address: leslie.leinwand@colorado.edu.
Discovery Institute · USSanford Burnham Prebys Medical Discovery Institute · USUniversity of Arizona · USUniversity of Colorado Boulder · US

Funding

REGULATION OF FATTY ACID OXIDATION DURING CARDIAC GROWTHR01HL058493 · NHLBI · WASHINGTON UNIVERSITY · PI KELLY, DANIEL PATRICK · 1998 to 2024
$10.6M
Molecular Control of Muscle Fuel MetabolismR01DK045416 · NIDDK · WASHINGTON UNIVERSITY · PI KELLY, DANIEL PATRICK · 1996 to 2020
$8.1M
Probing the Role of Mitochondrial Short-chain Carbon Homeostasis in the Hypertrophied and Failing HeartR01HL128349 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI MUOIO, DEBORAH M · 2016 to 2024
$6.1M
Molecular Characterization of Cardiomyopathy Mutations in Human Cardiac MyosinR01HL117138 · NHLBI · UNIVERSITY OF COLORADO · PI LEINWAND, LESLIE ANNE, PERKINS, THOMAS TUPPER · 2013 to 2021
$4.2M
Impact of AMP-activated kinase on sex differences in hypertrophic cardiomyopathyK02HL105799 · NHLBI · UNIVERSITY OF ARIZONA · PI KONHILAS, JOHN P · 2011 to 2015
$516k
NHLBI NIH HHS K02 HL105799NHLBI NIH HHS R01 HL058493NHLBI NIH HHS R01 HL117138NHLBI NIH HHS R01 HL128349NIDDK NIH HHS R01 DK045416
6 · The paper itself

Abstract

Exercise elicits coordinated multi-organ responses including skeletal muscle, vasculature, heart, and lung. In the short term, the output of the heart increases to meet the demand of strenuous exercise. Long-term exercise instigates remodeling of the heart including growth and adaptive molecular and cellular re-programming. Signaling pathways such as the insulin-like growth factor 1/PI3K/Akt pathway mediate many of these responses. Exercise-induced, or physiologic, cardiac growth contrasts with growth elicited by pathological stimuli such as hypertension. Comparing the molecular and cellular underpinnings of physiologic and pathologic cardiac growth has unveiled phenotype-specific signaling pathways and transcriptional regulatory programs. Studies suggest that exercise pathways likely antagonize pathological pathways, and exercise training is often recommended for patients with chronic stable heart failure or following myocardial infarction. Herein, we summarize the current understanding of the structural and functional cardiac responses to exercise as well as signaling pathways and downstream effector molecules responsible for these adaptations.

Indexed as

Metabolic Networks and PathwaysAnimalsCardiovascular DiseasesCardiovascular Physiological PhenomenaCardiovascular SystemExerciseGene Regulatory NetworksHeartHumansMyocardium

Identifiers

PMID28467921
PMCPMC5512429
OpenAlexW2610988715

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.