Evidence map›Paper›PMID 29600895›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2018

Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding.

Alan J Mouton, Osvaldo J Rivera, Merry L Lindsey

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
–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

55 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Ginsenoside RbJournal of pharmaceutical analysis · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Proteomics of the heart.Physiological reviews · 2024
    Review
  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

3 authors.

Alan J MoutonMississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center , Jackson, Mississippi.
Osvaldo J RiveraMississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center , Jackson, Mississippi.
Merry L LindseyMississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center , Jackson, Mississippi.ORCID 0000-0002-4090-0391

Funding

Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI COMPRETTA, CAROLINE E. · 2016 to 2025
$38.2M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
The Role of Macrophage-derived MMPs in LV RemodelingR01HL075360 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LINDSEY, MERRY L. · 2004 to 2018
$5.4M
Systems Biology of Fibroblast Activation Following Myocardial InfarctionR01HL129823 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LINDSEY, MERRY L. · 2016 to 2019
$1.5M
BLRD VA I01 BX000505NHLBI NIH HHS R01 HL075360NHLBI NIH HHS R01 HL129823NHLBI NIH HHS T32 HL105324NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

After myocardial infarction, remodeling of the left ventricle involves a wound-healing orchestra involving a variety of cell types. In order for wound healing to be optimal, appropriate communication must occur; these cells all need to come in at the right time, be activated at the right time in the right amount, and know when to exit at the right time. When this occurs, a new homeostasis is obtained within the infarct, such that infarct scar size and quality are sufficient to maintain left ventricular size and shape. The ideal scenario does not always occur in reality. Often, miscommunication can occur between infarct and remote spaces, across the temporal wound-healing spectrum, and across organs. When miscommunication occurs, adverse remodeling can progress to heart failure. This review discusses current knowledge gaps and recent development of the roles of inflammation and the extracellular matrix in myocardial infarction remodeling. In particular, the macrophage is one cell type that provides direct and indirect regulation of both the inflammatory and scar-forming responses. We summarize current research efforts focused on identifying biomarker indicators that reflect the status of each component of the wound-healing process to better predict outcomes.

Indexed as

Signal TransductionAnimalsExtracellular MatrixHeart FailureHumansMyocardial InfarctionMyocardiumextracellular matrixfibroblastinflammationmacrophageproteomicsscarsystems biology

Identifiers

PMID29600895
PMCPMC6087773

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.