Evidence map›Paper›PMID 27677409›Full record

ArticleNature communications2016

ANGPTL2 activity in cardiac pathologies accelerates heart failure by perturbing cardiac function and energy metabolism.

Zhe Tian, Keishi Miyata, Tsuyoshi Kadomatsu, Haruki Horiguchi, Hiroyuki Fukushima, Shugo Tohyama, Yoshihiro Ujihara, Takahiro Okumura, Satoshi Yamaguchi, Jiabin Zhao and 20 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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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

30 authors at 8 institutions in 2 countries.

Zhe TianDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Keishi MiyataDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Tsuyoshi KadomatsuDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Haruki HoriguchiDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Hiroyuki FukushimaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Shugo TohyamaDepartment of Cardiovascular Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan.
Yoshihiro UjiharaFirst Department of Physiology, Kawasaki Medical School, Okayama 701-092, Japan.
Takahiro OkumuraDepartment of Cardiology, Nagoya University Graduate school of Medicine, Nagoya 466-8550, Japan.
Satoshi YamaguchiDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Jiabin ZhaoDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Motoyoshi EndoDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Jun MorinagaDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Michio SatoDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Taichi SugizakiDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Shunshun ZhuDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Kazutoyo TeradaDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Hisashi SakaguchiDepartment of Cardiovascular Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Motohiro TakeyaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Naoki TakedaInstitute of Resource Developmental and Analysis, Kumamoto University, Kumamoto 860-8111, Japan.
Kimi ArakiInstitute of Resource Developmental and Analysis, Kumamoto University, Kumamoto 860-8111, Japan.
Ichiro ManabeDepartment of Aging Research, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Keiichi FukudaDepartment of Cardiovascular Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan.ORCID http://orcid.org/0000-0003-1413-0482
Kinya OtsuCardiovascular Division, King's College London British Heart Foundation Centre of Research Excellence, London SE5 9NU, UK.
Jun WadaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Toyoaki MuroharaDepartment of Cardiology, Nagoya University Graduate school of Medicine, Nagoya 466-8550, Japan.
Satoshi MohriFirst Department of Physiology, Kawasaki Medical School, Okayama 701-092, Japan.
Jun K YamashitaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto 606-8507, Japan.
Motoaki SanoDepartment of Cardiovascular Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan.
Yuichi OikeDepartment of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Kumamoto University · JPKeio University · JPKawasaki Medical School · JPKyoto University · JPNagoya University · JPOkayama University · JPChiba University · JPKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A cardioprotective response that alters ventricular contractility or promotes cardiomyocyte enlargement occurs with increased workload in conditions such as hypertension. When that response is excessive, pathological cardiac remodelling occurs, which can progress to heart failure, a leading cause of death worldwide. Mechanisms underlying this response are not fully understood. Here, we report that expression of angiopoietin-like protein 2 (ANGPTL2) increases in pathologically-remodeled hearts of mice and humans, while decreased cardiac ANGPTL2 expression occurs in physiological cardiac remodelling induced by endurance training in mice. Mice overexpressing ANGPTL2 in heart show cardiac dysfunction caused by both inactivation of AKT and sarco(endo)plasmic reticulum Ca

Identifiers

PMID27677409
PMCPMC5052800
OpenAlexW2525947787

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.