Evidence map›Paper›PMID 23365487›Full record

ReviewMediators of inflammation2013

Role of mitogen-activated protein kinase pathways in multifactorial adverse cardiac remodeling associated with metabolic syndrome.

Mohamed Asrih, François Mach, Alessio Nencioni, Franco Dallegri, Alessandra Quercioli, Fabrizio Montecucco

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Insulin-Heart Axis: Bridging Physiology to Insulin Resistance.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Review
  7. Neuropeptide Y attenuates cardiac remodeling and deterioration of function following myocardial infarction.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  8. Article
  9. Non-'classical' MEKs: A review of MEK3-7 inhibitors.Bioorganic & medicinal chemistry letters · 2020
    Review
  10. Article
  11. Role of mineralocorticoid receptor activation in cardiac diastolic dysfunction.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  12. Diabetic cardiomyopathy: where we are and where we are going.The Korean journal of internal medicine · 2017
    Review
  13. Article
  14. How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  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

6 authors at 2 institutions in 2 countries.

Mohamed AsrihDivision of Cardiology, Geneva University Hospital, Faculty of Medicine, Foundation for Medical Researches, Switzerland.
François Mach
Alessio Nencioni
Franco Dallegri
Alessandra Quercioli
Fabrizio Montecucco
Foundation for laboratory medicine · CHUniversity of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic syndrome has been widely associated with an increased risk for acute cardiovascular events. Emerging evidence supports metabolic syndrome as a condition favoring an adverse cardiac remodeling, which might evolve towards heart dysfunction and failure. This pathological remodeling has been described to result from the cardiac adaptive response to clinical mechanical conditions (such as hypertension, dyslipidemia, and hyperglycemia), soluble inflammatory molecules (such as cytokines and chemokines), as well as hormones (such as insulin), characterizing the pathophysiology of metabolic syndrome. Moreover, these cardiac processes (resulting in cardiac hypertrophy and fibrosis) are also associated with the modulation of intracellular signalling pathways within cardiomyocytes. Amongst the different intracellular kinases, mitogen-activated protein kinases (MAPKs) were shown to be involved in heart damage in metabolic syndrome. However, their role remains controversial. In this paper, we will discuss and update evidence on MAPK-mediated mechanisms underlying cardiac adverse remodeling associated with metabolic syndrome.

Indexed as

AnimalsCardiomegalyHumansMetabolic SyndromeMitogen-Activated Protein KinasesSignal TransductionMitogen-Activated Protein Kinases

Identifiers

PMID23365487
PMCPMC3556856
OpenAlexW2048564025

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.