Evidence map›Paper›PMID 31629566›Full record

ArticleInternational journal of cardiology2019

Angiotensin-(1-12)/chymase axis modulates cardiomyocyte L-type calcium currents in rats expressing human angiotensinogen.

Santiago Reyes, Che Ping Cheng, Drew J Roberts, Tomohisa Yamashita, Sarfaraz Ahmad, Jessica L VonCannon, Kendra N Wright, Louis J Dell'Italia, Jasmina Varagic, Carlos M Ferrario

Open access · greenAbstract read
In one paragraph

Article in International journal of cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 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

10 authors at 2 institutions in 1 country.

Santiago ReyesDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA. Electronic address: bmsarey@gmail.com.
Che Ping ChengDepartment of Internal Medicine, Section on Cardiovascular Medicine, Wake Forest School of Medicine, Winston Salem, NC, USA.
Drew J RobertsDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Tomohisa YamashitaDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Sarfaraz AhmadDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Jessica L VonCannonDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Kendra N WrightDepartment of Surgery, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Louis J Dell'ItaliaBirmingham Veteran Affairs Medical Center and Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL, USA.
Jasmina VaragicDepartment of Surgery and Cardiovascular Sciences Center, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Carlos M FerrarioDepartments of Surgery, Physiology and Pharmacology, and Social Sciences, Division of Public Health, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Wake Forest University · USUniversity of Alabama at Birmingham · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
New Molecular Target for Cardiac AgingR01AG049770 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHENG, HENG-JIE · 2015 to 2019
$1.6M
Angiotensin (1-12) and Hypertension in the ElderlyR21AG070371 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FERRARIO, CARLOS M · 2021 to 2022
$426k
NHLBI NIH HHS P01 HL051952NIA NIH HHS R01 AG049770NIA NIH HHS R21 AG070371NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

backgroundActivation of the intracrine renin angiotensin systems (RAS) is increasingly recognized as contributing to human pathologies, yet non-canonical renin-independent mechanisms for angiotensin II (Ang II) biosynthesis remain controversial. Direct Ang II generation from angiotensin-(1-12) [Ang-(1-12)] by chymase is an essential intracrine source for regulation of cardiac function. Using a transgenic rat model that overexpresses the human angiotensinogen gene [TGR(hAGT)L1623] and displays increased cardiac Ang II levels, this study aimed to provide evidence for intracrine activation of L-type calcium currents (I METHODS AND

resultsOn patch clamp, I

conclusionsOur data demonstrate the existence in cardiomyocytes of a calcium channel modulatory activity responsive to Ang II generated by the Ang-(1-12)/chymase axis that signals via intracellular receptors. Chronically elevated Ang II in TGR(hAGT)L1623 hearts leading to increased intracellular calcium through I

Indexed as

Angiotensin IAngiotensinogenAnimalsCalcium Channels, L-TypeCell Culture TechniquesChymasesMyocytes, CardiacPatch-Clamp TechniquesPeptide FragmentsRatsRats, Sprague-DawleyRats, TransgenicAngiotensin IAngiotensinogenCalcium Channels, L-TypeChymasesPeptide Fragmentsproangiotensin-12, ratAng-(1–12)Ang IIAngiotensin II type 1 receptorChymaseHypertensionHypertrophy

Identifiers

PMID31629566
PMCPMC6939452
OpenAlexW2980265256

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.