Evidence map›Paper›PMID 20407820›Full record

ReviewHeart failure reviews2011

STAT3 and cardiac remodeling.

Arash Haghikia, Britta Stapel, Melanie Hoch, Denise Hilfiker-Kleiner

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.5field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The βCirculation research · 2025
    Article
  5. Article
  6. The two-pore KAmerican journal of physiology. Heart and circulatory physiology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Perspective: mitochondrial STAT3 in cardioprotection.Basic research in cardiology · 2023
    Review
  13. Cardiovascular manifestations of inflammatory bowel diseases and the underlying pathogenic mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Angiotensin II blockers improve cardiac coronary flow under hemodynamic pressure overload.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    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

4 authors at 1 institution in 1 country.

Arash HaghikiaDepartment of Cardiology and Angiology, Medical School Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Britta Stapel
Melanie Hoch
Denise Hilfiker-Kleiner
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple in vitro and in vivo studies showed that the signal transducer and activator of transcription 3 (STAT3) protein is involved in cardiomyocyte protection and hypertrophy and via paracrine pathways impacts on the non-myocyte compartment, i.e., the vasculature and the extracellular matrix. In this regard, STAT3 interacts with a broad range of cellular and molecular mechanisms that direct remodeling processes in cardiac physiology (exercise, pregnancy) and pathophysiology (pressure overload, ischemia/reperfusion, myocardial infarction, and cardiotoxic agents). STAT3 is constitutively activated by a multitude of factors including cytokines, growth factors, neurohormones, mechanical load, and ischemia. It acts as a signaling molecule, a transcription factor and according to latest observations as a mitochondrial protein involved in energy production. In this review, we provide an overview on STAT3 signaling and summarize the current understanding of the role of STAT3 for different aspects of cardiac remodeling obtained from numerous experimental and clinical studies. Finally, we highlight and critically discuss STAT3 signaling as a possible target for future therapeutic approaches in the setting of cardiac remodeling.

Indexed as

STAT3 Transcription FactorVentricular RemodelingAgingAngiotensin IICardiomyopathy, DilatedExtracellular MatrixHumansInflammationMitochondriaMyocardiumMyocytes, CardiacSignal TransductionAngiotensin IISTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID20407820
OpenAlexW2006245789

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.