Evidence map›Paper›PMID 23054657›Full record

ReviewJournal of cardiovascular translational research2012

Crosstalk between the renin-angiotensin system and the advance glycation end product axis in the heart: role of the cardiac fibroblast.

Katrina Go Yamazaki, Eileen Gonzalez, Alexander C Zambon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Hypertension in diabetes.Pediatric nephrology (Berlin, Germany) · 2024
    Article
  2. Article
  3. Article
  4. Fibrosis in Chronic Kidney Disease: Pathogenesis and Consequences.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Do Advanced Glycation End Products and Its Receptor Play a Role in Pathophysiology of Hypertension?The International journal of angiology : official publication of the International College of Angiology, Inc · 2017
    Review
  14. EFFECT OF TRIPTOLIDE ON PROLIFERATION AND APOPTOSIS OF ANGIOTENSIN II-INDUCED CARDIAC FIBROBLASTSAfrican journal of traditional, complementary, and alternative medicines : AJTCAM · 2017
    Article
  15. Article
  16. Integrins and integrin-related proteins in cardiac fibrosis.Journal of molecular and cellular cardiology · 2016
    Review
  17. Article
  18. Review
  19. Review
  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 2 institutions in 1 country.

Katrina Go YamazakiDepartment of Biological Sciences, California State University Los Angeles, 5151 State University Dr ASCL 312, Los Angeles, CA, USA. kyamaza@calstatela.edu
Eileen Gonzalez
Alexander C Zambon
California State University Los Angeles · USUniversity of California, San Diego · US

Funding

San Diego Clinical and Translational Research InstituteUL1TR000100 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2012 to 2015
$19.7M
NCATS NIH HHS 8UL1TR000100-03NIGMS NIH HHS GM06852PHITPO CDC HHS 1U54HK08460-01
6 · The paper itself

Abstract

Cardiac fibroblasts (CFs) are involved in maintaining extracellular matrix (ECM) homeostasis in the heart. CFs mediate responses to hormonal and mechanical stimuli and relay these to other local cell types through release of autocrine and/or paracrine factors. CFs also play important roles in the setting of injury, i.e., myocardial infarction, where ECM production is key to efficient scarring. However, conditions exist in which excess production of ECM by CFs can lead to cardiac fibrosis. Two important pathways known to be involved in development of cardiac fibrosis are renin-angiotensin system (RAS) and advanced glycation end products (AGE) receptor (RAGE) signaling cascades. This report summarizes actions of these two pathways on function of CFs. Because cardiac fibrosis is an important component of diabetic cardiomyopathy, we include new data that suggests a possible crosstalk between the RAS and AGE/RAGE pathway in order to activate CFs in diabetes.

Indexed as

Receptor Cross-TalkRenin-Angiotensin SystemSignal TransductionAnimalsDiabetic CardiomyopathiesExtracellular MatrixFibroblastsFibrosisGlycation End Products, AdvancedHumansMyocardiumReceptor for Advanced Glycation End ProductsReceptors, ImmunologicGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsReceptors, Immunologic

Identifiers

PMID23054657
OpenAlexW2086608623

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.