Evidence map›Paper›PMID 29057165›Full record

ArticleCurrent pathobiology reports2017

Mechanisms of Fibroblast Activation in the Remodeling Myocardium.

Arti V Shinde, Nikolaos G Frangogiannis

Abstract read
In one paragraph

Article in Current pathobiology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Article
  2. Article
  3. Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  4. Article
  5. Review
  6. Spatial FAP Expression as Detected byMolecular imaging and biology · 2025
    Article
  7. Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025
    Review
  8. Matricellular protein CCN1 promotes collagen alignment and scar integrity after myocardial infarction.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Article
  9. Review
  10. Article
  11. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Asporin, an extracellular matrix protein, is a beneficial regulator of cardiac remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. Review
  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

2 authors.

Arti V ShindeThe Wilf Family Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx NY.
Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx NY.

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

purpose of reviewActivated fibroblasts are critically implicated in repair and remodeling of the injured heart. This manuscript discusses recent progress in the cell biology of fibroblasts in the infarcted and remodeling myocardium, highlighting advances in understanding the origin, function and mechanisms of activation of these cells. RECENT

findingsFollowing myocardial injury, fibroblasts undergo activation and myofibroblast transdifferentiation. Recently published studies have suggested that most activated myofibroblasts in the infarcted and pressure-overloaded hearts are derived from resident fibroblast populations. In the healing infarct, fibroblasts undergo dynamic phenotypic alterations in response to changes in the cytokine milieu and in the composition of the extracellular matrix. Fibroblasts do not simply serve as matrix-producing cells, but may also regulate inflammation, modulate cardiomyocyte survival and function, mediate angiogenesis, and contribute to phagocytosis of dead cells. SUMMARY: In the injured myocardium, fibroblasts are derived predominantly from resident populations and serve a wide range of functions.

Indexed as

cardiac remodelingcytokinefibroblastmyocardial infarctionmyofibroblast

Identifiers

PMID29057165
PMCPMC5646705

What OpenQuestion holds

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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.