Evidence map›Paper›PMID 19074585›Full record

ArticleEndocrinology2009

Thyroid hormone receptor-beta is associated with coronary angiogenesis during pathological cardiac hypertrophy.

Ayako Makino, Jorge Suarez, Hong Wang, Darrell D Belke, Brian T Scott, Wolfgang H Dillmann

Open access · greenAbstract read
In one paragraph

Article in Endocrinology, 2009. 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
2.5field-weighted citation impact, top 11% 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, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Cardioprotection and thyroid hormones.Heart failure reviews · 2016
    Review
  7. Role of thyroid hormones in ventricular remodeling.Current heart failure reports · 2015
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Inappropriate heat dissipation ignites brown fat thermogenesis in mice with a mutant thyroid hormone receptor α1.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  14. VDAC: old protein with new roles in diabetes.American journal of physiology. Cell physiology · 2012
    Article
  15. Article
  16. Review
  17. Thyroid hormone receptor-α and vascular function.American journal of physiology. Cell physiology · 2012
    Article
  18. Article
  19. Review
  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 1 institution in 1 country.

Ayako MakinoDepartment of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla, California 92093-0618, USA. wdillmann@ucsd.edu.
Jorge Suarez
Hong Wang
Darrell D Belke
Brian T Scott
Wolfgang H Dillmann
University of California, San Diego · US

Funding

Heart Failure and Thyroid HormoneR01HL089938 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DILLMANN, WOLFGANG H · 2007 to 2010
$1.5M
Mechanisms of coronary endothelial dysfunction in diabetesK01DK083506 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAKINO, AYAKO · 2009 to 2011
$366k
NHLBI NIH HHS HL89938NHLBI NIH HHS R01 HL089938NIDDK NIH HHS K01 DK083506
6 · The paper itself

Abstract

Insufficient angiogenesis is one of the causes leading to tissue ischemia and dysfunction. In heart failure, there is increasing evidence showing decreased capillary density in the left ventricle (LV) myocardium, although the detailed mechanisms contributing to it are not clear. The goal of this study was to investigate the role of thyroid hormone receptors (TRs) in the coronary microvascular rarefaction under pathological cardiac hypertrophy. The LV from hypertrophied/failing hearts induced by ascending aortic constriction (AAC) exhibited severe microvascular rarefaction, and this phenomenon was restored by chronic T(3) administration. Coronary endothelial cells (ECs) isolated from AAC hearts expressed lower TRbeta mRNA than control ECs, and chronic T(3) administration restored TRbeta mRNA expression level in AAC hearts to the control level. Among different TR subtype-specific knockout mice, TRbeta knockout and TRalpha/TRbeta double-knockout mice both exhibited significantly less capillary density in LV compared with wild-type mice. In vitro, coronary ECs isolated from TRbeta knockout mice lacked the ability to form capillary networks. In addition, we identified that kinase insert domain protein receptor/fetal liver kinase-1 (vascular endothelial growth factor-2 receptor) was one of the angiogenic mediators controlled by T(3) administration in the AAC heart. These data suggest that TRbeta in the coronary ECs regulates capillary density during cardiac development, and down-regulation of TRbeta results in coronary microvascular rarefaction during pathological hypertrophy.

Indexed as

AnimalsBlotting, WesternCardiomegalyCoronary VesselsEndothelial CellsHeart VentriclesMaleMiceMice, KnockoutMyocardiumNeovascularization, PathologicRatsRats, Sprague-DawleyThyroid Hormone Receptors betaTriiodothyronineThyroid Hormone Receptors betaTriiodothyronine

Identifiers

PMID19074585
PMCPMC2659277
OpenAlexW2134112099

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.