Evidence map›Paper›PMID 22825686›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2012

Pressure overload-induced cardiac remodeling and dysfunction in the absence of interleukin 6 in mice.

N Chin Lai, Mei Hua Gao, Eric Tang, Ruoying Tang, Tracy Guo, Nancy D Dalton, Aihua Deng, Tong Tang

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-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

31 citing papers in PubMed, 53 citations in OpenAlex.

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  7. Deficiency of Tregs in hypertension-associated left ventricular hypertrophy.Journal of clinical hypertension (Greenwich, Conn.) · 2023
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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

8 authors at 2 institutions in 1 country.

N Chin LaiDepartment of Medicine, University of California San Diego, VA San Diego Healthcare System, San Diego, CA, USA.
Mei Hua Gao
Eric Tang
Ruoying Tang
Tracy Guo
Nancy D Dalton
Aihua Deng
Tong Tang
University of California, San Diego · USVA San Diego Healthcare System · US

Funding

Vector Production CoreP01HL066941 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI FARQUHAR, MARILYN GIST · 2001 to 2017
$34.8M
Mechanisms of Adenylyl Cyclase Effects in the HeartR01HL081741 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI HAMMOND, H. KIRK · 2005 to 2013
$2.8M
Translational Studies of AAV Gene Transfer for CHFR01HL088426 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI HAMMOND, H. KIRK · 2008 to 2011
$1.4M
NHLBI NIH HHS P01 HL066941NHLBI NIH HHS R01 HL081741NHLBI NIH HHS R01 HL088426
6 · The paper itself

Abstract

Congestive heart failure is associated with increased expression of pro-inflammatory cytokines, and the levels of these cytokines correlate with heart failure severity and prognosis. Chronic interleukin 6 (IL-6) stimulation leads to left ventricular (LV) hypertrophy and dysfunction, and deletion of IL-6 reduces LV hypertrophy after angiotensin II infusion. In this study, we tested the hypothesis that IL-6 deletion has favorable effects on pressure-overloaded hearts. We performed transverse aortic constriction on IL-6-deleted (IL6KO) mice and C57BL/6J mice (CON) to induce pressure overload. Pressure overload was associated with similar LV hypertrophy, dilation, and dysfunction in CON and IL6KO mice. Re-activation of the fetal gene program was also similar in pressure-overloaded CON and IL6KO mice. There were no differences between CON and IL6KO mice in LV fibrosis or expression of extracellular matrix proteins after pressure overload. In addition, no group differences in apoptosis or autophagy were seen. These data indicate that IL-6 deletion does not block LV remodeling and dysfunction induced by pressure overload. Attenuated content of IL-11 appears to be a compensatory mechanism for IL-6 deletion in pressure-overloaded hearts. We infer from these data that limiting availability of IL-6 alone is not sufficient to attenuate LV remodeling and dysfunction in failing hearts.

Indexed as

Ventricular RemodelingAnimalsApoptosisAutophagyFemaleFibrosisHeart VentriclesHypertrophy, Left VentricularInterleukin-6MaleMiceMice, Inbred C57BLMice, KnockoutPressureSTAT3 Transcription FactorInterleukin-6Stat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID22825686
PMCPMC3482286
OpenAlexW2068782596

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.