Evidence map›Paper›PMID 26721917›Full record

ArticleCirculation. Heart failure2016

Heart Failure With Preserved Ejection Fraction Induces Beiging in Adipose Tissue.

María Valero-Muñoz, Shanpeng Li, Richard M Wilson, Maarten Hulsmans, Tamar Aprahamian, José J Fuster, Matthias Nahrendorf, Philipp E Scherer, Flora Sam

Open access · greenAbstract read
In one paragraph

Article in Circulation. Heart failure, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Metabolic dysregulation in the heart in obesity-associated HFpEF.Frontiers in cardiovascular medicine · 2025
    Article
  11. Early pathological mechanisms in a mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The immunology of heart failure with preserved ejection fraction.Clinical science (London, England : 1979) · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors at 3 institutions in 1 country.

María Valero-MuñozFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Shanpeng LiFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Richard M WilsonFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Maarten HulsmansFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Tamar AprahamianFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
José J FusterFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Matthias NahrendorfFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Philipp E SchererFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA.
Flora SamFrom the Whitaker Cardiovascular Institute, Boston University School of Medicine, MA (M.V.-M., S.L., R.M.W., T.A., J.J.F., F.S.); Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston (M.H., M.N.); Departments of Internal Medicine and Cell Biology, Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas (P.E.S.); and Cardiovascular Section (F.S.) and Evans Department of Internal Medicine (T.A., F.S.), Boston University School of Medicine, MA. flora.sam@bmc.org.
Harvard University · USMassachusetts General Hospital · USCenter for Systems Biology · US

Funding

Role of Aldosterone and Adiponectin in Inter-Tissue Communication in Diastolic HeR01HL117153 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2013 to 2016
$1.6M
NHLBI NIH HHS HL117153NHLBI NIH HHS R01 HL117153
6 · The paper itself

Abstract

backgroundDespite the increasing prevalence of heart failure with preserved ejection fraction (HFpEF) in humans, there are no evidence-based therapies for HFpEF. Clinical studies suggest a relationship between obesity-associated dysfunctional adipose tissue (AT) and HFpEF. However, an apparent obesity paradox exists in some HF populations with a higher body mass index. We sought to determine whether HFpEF exerted effects on AT and investigated the involved mechanisms. METHODS AND

resultsMice underwent d-aldosterone infusion, uninephrectomy, and were given 1% saline for 4 weeks. HFpEF mice developed hypertension, left ventricular hypertrophy, and diastolic dysfunction and had higher myocardial natriuretic peptide expression. Although body weights were similar in HFpEF and sham-operated mice, white AT was significantly smaller in HFpEF than in sham (epididymal AT, 7.59 versus 10.67 mg/g; inguinal AT, 6.34 versus 8.38 mg/g). These changes were associated with smaller adipocyte size and increased beiging markers (ucp-1, cidea, and eva) in white AT. Similar findings were seen in HFpEF induced by transverse aortic constriction. Increased activation of natriuretic peptide signaling was seen in white AT of HFpEF mice. The ratio of the signaling receptor, natriuretic peptide receptor type A, to the clearance receptor, nprc, was increased as was p38 mitogen-activated protein kinase activation. However, HFpEF mice failed to regulate body temperature during cold temperature exposure. In HFpEF, despite a larger brown AT mass (5.96 versus 4.50 mg/g), brown AT showed reduced activity with decreased uncoupling protein 1 (ucp-1), cell death-inducing DFFA-like effector a (cidea), and epithelial V-like antigen (eva) expression and decreased expression of lipolytic enzymes (hormone-sensitive lipase, lipoprotein lipase, and fatty acid binding protein 4) versus sham.

conclusionsThese findings show that HFpEF is associated with beiging in white AT and with dysfunctional brown AT.

Indexed as

Stroke VolumeVentricular Function, LeftAdipocytes, BrownAdipocytes, WhiteAdipose Tissue, BrownAdipose Tissue, WhiteAldosteroneAnimalsBiomarkersBody Temperature RegulationDisease Models, AnimalFibrosisHeart FailureHypertensionHypertrophy, Left VentricularInflammation MediatorsAldosteroneBiomarkersInflammation Mediatorsbrown adipose tissuediastolic heart failurenatriuretic peptideswhite adipose tissue

Identifiers

PMID26721917
PMCPMC4698901
OpenAlexW2209570399

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.