Evidence map›Paper›PMID 24993042›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Discoidin domain receptor 2 germline gene deletion leads to altered heart structure and function in the mouse.

Randy T Cowling, Seon Ju Yeo, In Jai Kim, Joong Il Park, Yusu Gu, Nancy D Dalton, Kirk L Peterson, Barry H Greenberg

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Discoid Domain Receptors Signaling in Macrophages-Mediated Diseases.International journal of general medicine · 2025
    Review
  2. Article
  3. Review
  4. Article
  5. The Pathogenesis of Cardiac Fibrosis: A Review of Recent Progress.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Cpxm2 as a novel candidate for cardiac hypertrophy and failure in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Cardiac fibroblasts: more than mechanical support.Journal of thoracic disease · 2017
    Review
  19. 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

8 authors at 1 institution in 1 country.

Randy T CowlingDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California rcowling@ucsd.edu.
Seon Ju YeoDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
In Jai KimDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
Joong Il ParkDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
Yusu GuDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
Nancy D DaltonDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
Kirk L PetersonDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
Barry H GreenbergDivision of Cardiology, Department of Medicine, University of California-San Diego, La Jolla, California.
University of California, San Diego · US

Funding

Development of Mouse Model to Study Fibroblast FunctionsR21HL080358 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI COWLING, RANDY T · 2006 to 2007
$419k
NHLBI NIH HHS R21 HL080358NHLBI NIH HHS R21-HL-080358
6 · The paper itself

Abstract

Discoidin domain receptor 2 (DDR2) is a fibrillar collagen receptor that is expressed in mesenchymal cells throughout the body. In the heart, DDR2 is selectively expressed on cardiac fibroblasts. We generated a germline DDR2 knockout mouse and used this mouse to examine the role of DDR2 deletion on heart structure and function. Echocardiographic measurements from null mice were consistent with those from a smaller heart, with reduced left ventricular chamber dimensions and little change in wall thickness. Fractional shortening appeared normal. Left ventricular pressure measurements revealed mild inotropic and lusitropic abnormalities that were accentuated by dobutamine infusion. Both body and heart weights from 10-wk-old male mice were ~20% smaller in null mice. The reduced heart size was not simply due to reduced body weight, since cardiomyocyte lengths were atypically shorter in null mice. Although normalized cardiac collagen mass (assayed by hydroxyproline content) was not different in null mice, the collagen area fraction was statistically higher, suggesting a reduced collagen density from altered collagen deposition and cross-linking. Cultured cardiac fibroblasts from null mice deposited collagen at a slower rate than wild-type littermates, possibly due to the expression of lower prolyl 4-hydroxylase α-isoform 1 enzyme levels. We conclude that genetic deletion of the DDR2 collagen receptor alters cardiac fibroblast function. The resulting perturbations in collagen deposition can influence the structure and function of mature cardiomyocytes.

Indexed as

Gene DeletionGerm-Line MutationVentricular FunctionAmino Acid SequenceAnimalsCells, CulturedCollagenDiscoidin Domain ReceptorsDobutamineEchocardiographyHeart VentriclesMaleMiceMolecular Sequence DataMyocardiumMyocytes, CardiacCollagenDiscoidin Domain ReceptorsDobutamineReceptor Protein-Tyrosine KinasesReceptors, Mitogencardiaccollagen depositioncollagen receptordevelopmentfibroblast

Identifiers

PMID24993042
PMCPMC4187391
OpenAlexW2041981225

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.