Evidence map›Paper›PMID 28826664›Full record

ArticleJournal of molecular and cellular cardiology2017

Aicar treatment reduces interstitial fibrosis in aging mice: Suppression of the inflammatory fibroblast.

Katarzyna A Cieslik, JoAnn Trial, Mark L Entman

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Article
  9. Review
  10. Sex-specific phenotypes in the aging mouse heart and consequences for chronic fibrosis.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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  17. Targeting Mitochondrial Network Architecture in Down Syndrome and Aging.International journal of molecular sciences · 2020
    Review
  18. Roles of AMP-Activated Protein Kinase (AMPK) in Mammalian Reproduction.Frontiers in cell and developmental biology · 2020
    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 1 institution in 1 country.

Katarzyna A CieslikDivision of Cardiovascular Sciences, DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, TX, United States; Houston Methodist Hospital, Houston, TX, United States.
JoAnn TrialDivision of Cardiovascular Sciences, DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, TX, United States; Houston Methodist Hospital, Houston, TX, United States.
Mark L EntmanDivision of Cardiovascular Sciences, DeBakey Heart Center, Department of Medicine, Baylor College of Medicine, Houston, TX, United States; Houston Methodist Hospital, Houston, TX, United States. Electronic address: mentman@bcm.edu.
Methodist Hospital · US

Funding

Role of Blood-Borne Fibroblast Precursors in Ischemic CardiomyopathyR01HL089792 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ENTMAN, MARK L · 2007 to 2016
$3.4M
NHLBI NIH HHS R01 HL089792
6 · The paper itself

Abstract

In 2030, elderly people will represent 20% of the United States population. Even now, chronic cardiac diseases, especially heart failure with preserved systolic function (HFpEF), are the most expensive DRGs for Medicare. Progressive interstitial fibrosis in the aging heart is well recognized as an important component of HFpEF. Our recent studies suggested an important pathophysiologic role for reduced TGF-β receptor 1 (TGFβR1) signaling in mesenchymal stem cells (MSCs) and their mesenchymal fibroblast progeny in the development of interstitial fibrosis. This report arises from our previous studies, which suggest that an inflammatory phenotype exists in these mesenchymal fibroblasts as a result of a reduced TGF-β-Smad-dependent pathway but upregulated farnesyltransferase (FTase)-Ras-Erk signaling. In this report we provide evidence for a therapeutic approach that downregulates Erk activation through an adenosine monophosphate-activated kinase (AMPK) pathway. Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period. This treatment suppressed excessive monocyte chemoattractant protein-1 (MCP-1) generation, which diminished leukocyte infiltration and in consequence suppressed the formation of macrophage-derived myeloid fibroblasts. Interestingly, the number of mesenchymal fibroblasts was also reduced. In addition, we observed changes in extracellular matrix (ECM) deposition, specifically that collagen type I and the alternatively spliced variant of fibronectin (EDA) expressions were reduced. These data suggest that the upregulation of AMPK activity is a potential therapeutic approach to fibrosis in the aging heart.

Indexed as

AgingAminoimidazole CarboxamideAnimalsBiomarkersCell CountFibroblastsFibrosisInflammationMaleMice, Inbred C57BLMyocardiumRibonucleotidesAICA ribonucleotideAminoimidazole CarboxamideBiomarkersRibonucleotidesAMPKFibroblastFibrosisHeartMacrophage

Identifiers

PMID28826664
PMCPMC5600709
OpenAlexW2745169363

What OpenQuestion holds

Textmetadata
LicenceTDM
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.