Evidence map›Paper›PMID 27081162›Full record

ArticlePhysiological reports2016

N-acetylcysteine attenuates the development of cardiac fibrosis and remodeling in a mouse model of heart failure.

Beverly Giam, Po-Yin Chu, Sanjaya Kuruppu, A Ian Smith, Duncan Horlock, Helen Kiriazis, Xiao-Jun Du, David M Kaye, Niwanthi W Rajapakse

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  14. The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Oxidative Stress in Cell Death and Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2019
    Review
  20. 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

9 authors at 2 institutions in 1 country.

Beverly GiamBaker IDI Heart and Diabetes Institute, Melbourne, Australia Central Clinical School, Monash University, Melbourne, Australia beverly.giam@bakeridi.edu.au.
Po-Yin ChuBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Sanjaya KuruppuDepartment of Biochemistry, Monash University, Melbourne, Australia.
A Ian SmithDepartment of Biochemistry, Monash University, Melbourne, Australia.
Duncan HorlockBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Helen KiriazisBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Xiao-Jun DuBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
David M KayeBaker IDI Heart and Diabetes Institute, Melbourne, Australia Department of Medicine, Monash University, Melbourne, Australia.
Niwanthi W RajapakseBaker IDI Heart and Diabetes Institute, Melbourne, Australia Department of Physiology, Monash University, Melbourne, Australia.
Monash University · AUBaker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress plays a central role in the pathogenesis of heart failure. We aimed to determine whether the antioxidantN-acetylcysteine can attenuate cardiac fibrosis and remodeling in a mouse model of heart failure. Minipumps were implanted subcutaneously in wild-type mice (n = 20) and mice with cardiomyopathy secondary to cardiac specific overexpression of mammalian sterile 20-like kinase 1 (MST-1;n = 18) to administerN-acetylcysteine (40 mg/kg per day) or saline for a period of 8 weeks. At the end of this period, cardiac remodeling and function was assessed via echocardiography. Fibrosis, oxidative stress, and expression of collagen types I andIIIwere quantified in heart tissues. Cardiac perivascular and interstitial fibrosis were greater by 114% and 209%, respectively, inMST-1 compared to wild type (P ≤ 0.001). InMST-1 mice administeredN-acetylcysteine, perivascular and interstitial fibrosis were 40% and 57% less, respectively, compared to those treated with saline (P ≤ 0. 03). Cardiac oxidative stress was 119% greater inMST-1 than in wild type (P < 0.001) andN-acetylcysteine attenuated oxidative stress inMST-1 by 42% (P = 0.005). These data indicate thatN-acetylcysteine can blunt cardiac fibrosis and related remodeling in the setting of heart failure potentially by reducing oxidative stress. This study provides the basis to investigate the role ofN-acetylcysteine in chronic heart failure.

Indexed as

AcetylcysteineAnimalsAntioxidantsCollagen Type ICollagen Type IIIDisease Models, AnimalFibrosisGenetic Predisposition to DiseaseHeart FailureMaleMice, Inbred C57BLMice, TransgenicMyocytes, CardiacOxidative StressPhenotypeProtein Serine-Threonine KinasesAcetylcysteineAntioxidantsCollagen Type ICollagen Type IIIProtein Serine-Threonine KinasesFibrosisheart failureN‐acetylcysteineoxidative stress

Identifiers

PMID27081162
PMCPMC4831326
OpenAlexW2338101599

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.