Evidence map›Paper›PMID 21918107›Full record

ArticleScience translational medicine2011

Donor myocardial infarction impairs the therapeutic potential of bone marrow cells by an interleukin-1-mediated inflammatory response.

Xiaoyin Wang, Junya Takagawa, Viola C Lam, Daniel J Haddad, Diana L Tobler, Pamela Y Mok, Yan Zhang, Brian T Clifford, Kranthi Pinnamaneni, Shereen A Saini and 8 more

Abstract read
In one paragraph

Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  15. A steroid receptor coactivator stimulator (MCB-613) attenuates adverse remodeling after myocardial infarction.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  18. G-CSF's Last Stand in STEMI.Circulation research · 2019
    Article
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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

18 authors at 2 institutions in 1 country.

Xiaoyin WangCardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
Junya Takagawa
Viola C Lam
Daniel J Haddad
Diana L Tobler
Pamela Y Mok
Yan Zhang
Brian T Clifford
Kranthi Pinnamaneni
Shereen A Saini
Robert Su
Maya J Bartel
Richard E Sievers
Larry Carbone
Scott Kogan
Yerem Yeghiazarians
Michelle Hermiston
Matthew L Springer
University of California, San Francisco · USBroad Center · US

Funding

The Role of Nitric Oxide Synthase in Circulating Progenitor Cell FunctionR01HL086917 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPRINGER, MATTHEW LAWRENCE · 2007 to 2011
$2.1M
Bone marrow cell therapy for cardiac disease: Impact of donor age and infarctionR21HL097129 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPRINGER, MATTHEW LAWRENCE · 2010 to 2011
$425k
Closed-Chest Cell Injections into Mouse Myocardium Targeted by UltrasoundR03EB005802 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPRINGER, MATTHEW LAWRENCE · 2005 to 2006
$150k
NHLBI NIH HHS R01 HL086917NHLBI NIH HHS R21 HL097129NIBIB NIH HHS R03 EB005802
6 · The paper itself

Abstract

Delivery of bone marrow cells (BMCs) to the heart has substantially improved cardiac function in most rodent models of myocardial infarction (MI), but clinical trials of BMC therapy have led to only modest improvements. Rodent models typically involve intramyocardial injection of BMCs from distinct donor individuals who are healthy. In contrast, autologous BMCs from individuals after MI are used for clinical trials. Using BMCs from donor mice after MI, we discovered that recent MI impaired BMC therapeutic efficacy. MI led to myocardial inflammation and an increased inflammatory state in the bone marrow, changing the BMC composition and reducing their efficacy. Injection of a general anti-inflammatory drug or a specific interleukin-1 inhibitor to donor mice after MI prevented this impairment. Our findings offer an explanation of why human trials have not matched the success of rodent experiments and suggest potential strategies to improve the success of clinical autologous BMC therapy.

Indexed as

Tissue DonorsAnimalsBone Marrow TransplantationEchocardiographyFlow CytometryInterleukin-1MaleMiceMice, Inbred C57BLMyocardial InfarctionInterleukin-1

Identifiers

PMID21918107
PMCPMC3350804
OpenAlexW2172126964

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.