Evidence map›Paper›PMID 32343958›Full record

ReviewThe American journal of pathology2020

Mouse Models of Heart Failure with Preserved or Reduced Ejection Fraction.

Natalie A Noll, Hind Lal, W David Merryman

Abstract readReview
In one paragraph

Review in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Article
  2. Review
  3. Low and High Pressor Doses of Ang II Lead to Two Distinct Phenotypes of Hypertensive Heart Disease in Mice.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. The role of sphingolipids in heart failure.European heart journal open · 2025
    Review
  11. Article
  12. Loss of glymphatic homeostasis in heart failure.Brain : a journal of neurology · 2025
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors.

Natalie A NollDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee.
Hind LalDepartment of Medicine, Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama.
W David MerrymanDepartment of Biomedical Engineering, Vanderbilt University, Nashville, Tennessee. Electronic address: david.merryman@vanderbilt.edu.

Funding

Mechanobiology of Cardiopulmonary FibrosisR35HL135790 · NHLBI · VANDERBILT UNIVERSITY · PI MERRYMAN, WILLIAM D · 2017 to 2023
$5.5M
Signaling Mechanisms Governing Myocardial Fibrosis in Diseased HeartR01HL133290 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Hind Lal · 2017 to 2026
$3.6M
Project-002R01HL143074 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Hind Lal · 2019 to 2026
$3.4M
Talin1 Function in Cardiac MyofibroblastsF31HL149168 · NHLBI · VANDERBILT UNIVERSITY · PI NOLL, NATALIE A · 2019 to 2022
$102k
NHLBI NIH HHS F31 HL149168NHLBI NIH HHS R01 HL133290NHLBI NIH HHS R01 HL143074NHLBI NIH HHS R35 HL135790
6 · The paper itself

Abstract

Heart failure (HF) is a chronic, complex condition with increasing incidence worldwide, necessitating the development of novel therapeutic strategies. This has led to the current clinical strategies, which only treat symptoms of HF without addressing the underlying causes. Multiple animal models have been developed in an attempt to recreate the chronic HF phenotype that arises following a variety of myocardial injuries. Although significant strides have been made in HF research, an understanding of more specific mechanisms will require distinguishing models that resemble HF with preserved ejection fraction (HFpEF) from those with reduced ejection fraction (HFrEF). Therefore, current mouse models of HF need to be re-assessed to determine which of them most closely recapitulate the specific etiology of HF being studied. This will allow for the development of therapies targeted specifically at HFpEF or HFrEF. This review will summarize the commonly used mouse models of HF and discuss which aspect of human HF each model replicates, focusing on whether HFpEF or HFrEF is induced, to allow better investigation into pathophysiological mechanisms and treatment strategies.

Indexed as

AnimalsDisease Models, AnimalHeart FailureMiceStroke VolumeVentricular Dysfunction, Left

Identifiers

PMID32343958
PMCPMC7416075

What OpenQuestion holds

Textmetadata
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.