Evidence map›Paper›PMID 24704539›Full record

ArticleJournal of cardiac failure2014

Analysis of skeletal muscle gene expression patterns and the impact of functional capacity in patients with systolic heart failure.

Daniel E Forman, Karla M Daniels, Lawrence P Cahalin, Alexandra Zavin, Kelly Allsup, Peirang Cao, Mahalakshmi Santhanam, Jacob Joseph, Ross Arena, Antonio Lazzari and 2 more

Abstract read
In one paragraph

Article in Journal of cardiac failure, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  5. Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Skeletal muscle alterations in HFrEF vs. HFpEF.Current heart failure reports · 2017
    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

12 authors at 7 institutions in 1 country.

Daniel E FormanNew England Geriatric Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, Boston, Massachusetts; Division of Cardiovascular Medicine, Veterans Affairs Boston Healthcare System, Boston, Massachusetts; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical, School, Boston, Massachusetts. Electronic address: deforman@partners.org.
Karla M DanielsDivision of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical, School, Boston, Massachusetts.
Lawrence P CahalinDepartment of Physical Therapy, Leonard M. Miller School of Medicine, University of Miami, Miami, Florida.
Alexandra ZavinNew England Geriatric Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, Boston, Massachusetts.
Kelly AllsupNew England Geriatric Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, Boston, Massachusetts.
Peirang CaoDivision of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Mahalakshmi SanthanamDivision of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
Jacob JosephDivision of Cardiovascular Medicine, Veterans Affairs Boston Healthcare System, Boston, Massachusetts; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical, School, Boston, Massachusetts.
Ross ArenaDepartment of Physical Therapy and Integrative Physiology Laboratory - College of Applied Health Sciences, University of Illinois Chicago, Chicago, Illinois.
Antonio LazzariDivision of Rheumatology, Veterans Affairs Boston Healthcare System, Boston, Massachusetts; Boston University School of Medicine, Boston, Massachusetts.
P Christian SchulzeDivision of Cardiovascular Medicine, Columbia University Medical Center, New York, New York.
Stewart H LeckerBoston University School of Medicine, Boston, Massachusetts.
Brigham and Women's Hospital · USBeth Israel Deaconess Medical Center · USBoston University · USGeriatric Research Education and Clinical Center · USColumbia University Irving Medical Center · USUniversity of Illinois Urbana-Champaign · USUniversity of Miami · US

Funding

Cardiac Lipotoxicity and Ceramide Metabolism in Heart FailureR01HL114813 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI COLOMBO, PAOLO C, SCHULZE, P. CHRISTIAN · 2013 to 2017
$3.0M
Cardiac and Skeletal Muscle Metabolism and Proteolysis in Heart FailureK23HL095742 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SCHULZE, P. CHRISTIAN · 2009 to 2013
$677k
NHLBI NIH HHS K23 HL095742NHLBI NIH HHS R01 HL114813
6 · The paper itself

Abstract

backgroundDeclining physical function is common among systolic heart failure (HF) patients and heralds poor clinical outcomes. We hypothesized that coordinated shifts in expression of ubiquitin-mediated atrophy-promoting genes are associated with muscle atrophy and contribute to decreased physical function.

methodsSystolic HF patients (left ventricular ejection fraction [LVEF] ≤40%) underwent skeletal muscle biopsies (nondominant vastus lateralis) and comprehensive physical assessments. Skeletal muscle gene expression was assessed with the use of real-time polymerase chain reaction. Aerobic function was assessed with the use of cardiopulmonary exercise and 6-minute walk tests. Strength capacity was assessed with the use of pneumatic leg press (maximum strength and power). Serologic inflammatory markers also were assessed.

results54 male patients (66.6 ± 10.0 years) were studied: 24 systolic HF patients (mean LVEF 28.9 ± 7.8%) and 30 age-matched control subjects. Aerobic and strength parameters were diminished in HF versus control. FoxO1 and FoxO3 were increased in HF versus control (7.9 ± 6.2 vs 5.0 ± 3.5, 6.5 ± 4.3 vs 4.3 ± 2.8 relative units, respectively; P ≤ .05 in both). However, atrogin-1 and MuRF-1 were similar in both groups. PGC-1α was also increased in HF (7.9 ± 5.4 vs. 5.3 ± 3.6 relative units; P < .05). Muscle levels of insulin-like growth factor (IGF) 1 as well as serum levels of tumor necrosis factor α, C-reactive protein, interleukin (IL) 1β, and IL-6 were similar in HF and control.

conclusionExpression of the atrophy-promoting genes FoxO1 and FoxO3 were increased in skeletal muscle in systolic HF compared with control, but other atrophy gene expression patterns (atrogin-1 and MuRF-1), as well as growth promoting patterns (IGF-1), were similar. PGC-1α, a gene critical in enhancing mitochondrial function and moderating FoxO activity, may play an important counterregulatory role to offset ubiquitin pathway-mediated functional decrements.

Indexed as

Gene Expression RegulationHospitals, VeteransAgedCohort StudiesCross-Sectional StudiesExercise TestHeart Failure, SystolicHumansMaleMiddle AgedMuscle, SkeletalMuscle StrengthStroke VolumeVentricular Function, Leftgene expressionHeart failureskeletal muscle

Identifiers

PMID24704539
PMCPMC4278433
OpenAlexW2057725149

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.