Evidence map›Paper›PMID 35626694›Full record

ReviewCells2022

Fibrotic Signaling in Cardiac Fibroblasts and Vascular Smooth Muscle Cells: The Dual Roles of Fibrosis in HFpEF and CAD.

Julian C Bachmann, Simon J Baumgart, Anna K Uryga, Markus H Bosteen, Giulia Borghetti, Michael Nyberg, Kate M Herum

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. MATR3 regulates METTL3-Mediated mJournal of bioenergetics and biomembranes · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Distribution and impact of p16Experimental & molecular medicine · 2024
    Article
  15. Heart failure with preserved ejection fraction.Nature reviews. Disease primers · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Ferroptosis in heart failure.Journal of molecular and cellular cardiology · 2022
    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

7 authors at 1 institution in 1 country.

Julian C BachmannResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Simon J BaumgartResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Anna K UrygaResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Markus H BosteenResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Giulia BorghettiResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Michael NybergResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.ORCID 0000-0002-3937-4697
Kate M HerumResearch and Early Development, Novo Nordisk A/S, Novo Nordisk Park, 2760 Maaloev, Denmark.
Novo Nordisk (Denmark) · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with heart failure with preserved ejection fraction (HFpEF) and atherosclerosis-driven coronary artery disease (CAD) will have ongoing fibrotic remodeling both in the myocardium and in atherosclerotic plaques. However, the functional consequences of fibrosis differ for each location. Thus, cardiac fibrosis leads to myocardial stiffening, thereby compromising cardiac function, while fibrotic remodeling stabilizes the atherosclerotic plaque, thereby reducing the risk of plaque rupture. Although there are currently no drugs targeting cardiac fibrosis, it is a field under intense investigation, and future drugs must take these considerations into account. To explore similarities and differences of fibrotic remodeling at these two locations of the heart, we review the signaling pathways that are activated in the main extracellular matrix (ECM)-producing cells, namely human cardiac fibroblasts (CFs) and vascular smooth muscle cells (VSMCs). Although these signaling pathways are highly overlapping and context-dependent, effects on ECM remodeling mainly act through two core signaling cascades: TGF-

Indexed as

Coronary Artery DiseaseHeart FailureFibroblastsFibrosisHumansMuscle, Smooth, VascularStroke VolumeAngiotensin IIatherosclerosiscardiac fibroblastextracellular matrixfibrous capheart failuresignalingTGF-βvascular smooth muscle cell

Identifiers

PMID35626694
PMCPMC9139546
OpenAlexW4280582026

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.