Evidence map›Paper›PMID 27496875›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Cardiac-deleterious role of galectin-3 in chronic angiotensin II-induced hypertension.

Germán E González, N-E Rhaleb, Martin A D'Ambrosio, Pablo Nakagawa, Tang-Dong Liao, Edward L Peterson, Pablo Leung, Xiangguo Dai, Branislava Janic, Yun-He Liu and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018
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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

12 authors at 2 institutions in 2 countries.

Germán E GonzálezHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
N-E RhalebHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Martin A D'AmbrosioHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Pablo NakagawaHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Tang-Dong LiaoHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Edward L PetersonDepartment of Public Health Sciences, Henry Ford Hospital, Detroit, Michigan.
Pablo LeungHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Xiangguo DaiHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Branislava JanicHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Yun-He LiuHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Xiao-Ping YangHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan.
Oscar A CarreteroHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan; ocarret1@hfhs.org.
Henry Ford Hospital · USUniversity of Buenos Aires · AR

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI ORTIZ, PABLO A. · 1985 to 2017
$39.8M
NHLBI NIH HHS P01 HL028982
6 · The paper itself

Abstract

Galectin-3 (Gal-3), a member of the β-galactoside lectin family, has an important role in immune regulation. In hypertensive rats and heart failure patients, Gal-3 is considered a marker for an unfavorable prognosis. Nevertheless, the role and mechanism of Gal-3 action in hypertension-induced target organ damage are unknown. We hypothesized that, in angiotensin II (ANG II)-induced hypertension, genetic deletion of Gal-3 prevents left ventricular (LV) adverse remodeling and LV dysfunction by reducing the innate immune responses and myocardial fibrosis. To induce hypertension, male C57BL/6J and Gal-3 knockout (KO) mice were infused with ANG II (3 μg·min

Indexed as

Angiotensin IIAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBlood PressureBlotting, WesternCardiomegalyCD68 MoleculeCytokinesDisease Models, AnimalEchocardiographyEnzyme-Linked Immunosorbent AssayFibrosisFlow CytometryGalectin 3HypertensionAngiotensin IIAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeCD68 protein, mouseCytokinesGalectin 3Icam1 protein, mouseIntercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1angiotensin IIfibrosisgalectin-3hypertensioninflammationinterleukin-6macrophages

Identifiers

PMID27496875
PMCPMC5130499
OpenAlexW2487643962

What OpenQuestion holds

Textmetadata
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.