Evidence map›Paper›PMID 30619368›Full record

ReviewFrontiers in immunology2018

Recent Developments on the Crosstalk Between STAT3 and Inflammation in Heart Function and Disease.

Mazen Kurdi, Carlos Zgheib, George W Booz

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Molecular targets and mechanisms ofWorld journal of diabetes · 2023
    Article
  11. Article
  12. Cardiovascular manifestations of inflammatory bowel diseases and the underlying pathogenic mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Review
  13. Article
  14. Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022
    Review
  15. Article
  16. Article
  17. Network Pharmacology andFrontiers in pharmacology · 2022
    Article
  18. Review
  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 at 3 institutions in 2 countries.

Mazen KurdiFaculty of Sciences, Department of Chemistry and Biochemistry, and The Laboratory of Experimental and Clinical Pharmacology, Lebanese University, Beirut, Lebanon.
Carlos ZgheibLaboratory for Fetal and Regenerative Biology, Department of Surgery, School of Medicine, University of Colorado Denver, Anschutz Medical Campus and Colorado Children's Hospital, Aurora, CO, United States.
George W BoozDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, United States.
Children's Hospital Colorado · USLebanese University · LBUniversity of Mississippi Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor STAT3 has a protective function in the heart. Until recently, the role of STAT3 in hypertension-induced cardiac hypertrophy was unsettled. Earlier studies revealed that global reduction of STAT3 activity reduced cardiac hypertrophy with hypertension, but caused a disruption of myofilaments and increased contractile dysfunction. However, newer studies with cardiomyocyte-specific deletion of STAT3 indicate that STAT3 does not cause cardiac hypertrophy with increased blood pressure. Rather, cardiac STAT3 is important for maintaining metabolic homeostasis, and loss of STAT3 in cardiomyocytes makes the heart more susceptible to chronic pathological insult, for example by disrupting glucose metabolism and protective signaling networks via the upregulation of certain microRNAs. This scenario has implications for understanding peripartum cardiomyopathy as well. In viral myocarditis, STAT3 opposes the initiation of the dilated phenotype by maintaining membrane integrity via the expression of dystrophin. STAT3 signaling was also found to attenuate myocarditis by polarizing macrophages to a less inflammatory phenotype. On the other hand, STAT3 contributes to immune-mediated myocarditis due to IL-6-induced complement component C3 production in the liver, as well as the differentiation of Th17 cells, which play a role in initiation and development of myocarditis. Besides canonical signaling pathways, unphosphorylated STAT3 (U-STAT3) and redox-activated STAT3 have been shown to couple to transcription in the heart. In addition, tissue signaling cytokines such as IL-22 and IL-17 have been proposed to have actions on the heart that involve STAT3, but are not fully defined. Understanding the novel and often protective aspects of STAT3 in the myocardium could lead to new therapeutic approaches to treat heart disease.

Indexed as

AnimalsCardiomegalyComplement C3Disease Models, AnimalHeartHumansInterleukin-17Interleukin-22Interleukin-6InterleukinsMacrophagesMyocarditisMyocardiumMyocytes, CardiacSignal TransductionSTAT3 Transcription FactorComplement C3Interleukin-17Interleukin-22Interleukin-6InterleukinsSTAT3 Transcription Factorcardiac remodelingcytokinesheart failureimmunitymyocarditisperipartum cardiomyopathy

Identifiers

PMID30619368
PMCPMC6305745
OpenAlexW2905088771

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.