Evidence map›Paper›PMID 24646609›Full record

ArticleGene therapy2014

Deletion of CXCR4 in cardiomyocytes exacerbates cardiac dysfunction following isoproterenol administration.

E R Wang, A A Jarrah, L Benard, J Chen, M Schwarzkopf, L Hadri, S T Tarzami

Open access · greenAbstract read
In one paragraph

Article in Gene therapy, 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
1.2field-weighted citation impact, top 20% 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, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023
    Review
  4. Article
  5. Article
  6. LncRNA TINCR improves cardiac hypertrophy by regulating the miR-211-3p-VEGFB-SDF-1α-CXCR4 pathway.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genome-Wide RNAi Screen Identifies Regulators of Cardiomyocyte Necrosis.ACS pharmacology & translational science · 2019
    Article
  14. CXCR4 Cardiac Specific Knockout Mice Develop a Progressive Cardiomyopathy.International journal of molecular sciences · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 1 institution in 1 country.

E R WangDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
A A JarrahDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
L BenardDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
J ChenDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
M SchwarzkopfDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
L HadriDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
S T TarzamiDepartment of Medicine, Division of Cardiovascular Research Center, Mount Sinai School of Medicine, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · US

Funding

Chemokine receptor-4 regulation of Beta adrenergic-mediated calcium channelK02HL102163 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI TARZAMI, SIMA T · 2010 to 2012
$205k
NHLBI NIH HHS K02 HL102163NHLBI NIH HHS K02HL102163-01
6 · The paper itself

Abstract

Altered alpha- and beta-adrenergic receptor signaling is associated with cardiac hypertrophy and failure. Stromal cell-derived factor-1α (SDF-1α) and its cognate receptor CXCR4 have been reported to mediate cardioprotection after injury through the mobilization of stem cells into injured tissue. However, little is known regarding whether SDF-1/CXCR4 induces acute protection following pathological hypertrophy and if so, by what molecular mechanism. We have previously reported that CXCR4 physically interacts with the beta-2 adrenergic receptor and modulates its downstream signaling. Here we have shown that CXCR4 expression prevents beta-adrenergic receptor-induced hypertrophy. Cardiac beta-adrenergic receptors were stimulated with the implantation of a subcutaneous osmotic pump administrating isoproterenol and CXCR4 expression was selectively abrogated in cardiomyocytes using Cre-loxP-mediated gene recombination. CXCR4 knockout mice showed worsened fractional shortening and ejection fraction. CXCR4 ablation increased susceptibility to isoproterenol-induced heart failure, by upregulating apoptotic markers and reducing mitochondrial function; cardiac function decreases whereas fibrosis increases. In addition, CXCR4 expression was rescued with the use of cardiotropic adeno-associated viral-9 vectors. CXCR4 gene transfer reduced cardiac apoptotic signaling, improved mitochondrial function and resulted in a recovered cardiac function. Our results represent the first evidence that SDF-1/CXCR4 signaling mediates acute cardioprotection through modulating beta-adrenergic receptor signaling in vivo.

Indexed as

Adrenergic beta-AgonistsAnimalsApoptosisCardiomegalyCardiotonic AgentsChemokine CXCL12DependovirusFibrosisGene Knockout TechniquesGenetic VectorsGene Transfer TechniquesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeart FailureIsoproterenolMiceAdrenergic beta-AgonistsCardiotonic AgentsChemokine CXCL12CXCR4 protein, mouseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIsoproterenolReceptors, Adrenergic, betaReceptors, CXCR4

Identifiers

PMID24646609
PMCPMC4016112
OpenAlexW1981963947

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.