Evidence map›Paper›PMID 35042831›Full record

ArticleMolecular pharmacology2022

A Recombinant Dimethylarginine Dimethylaminohydrolase-1-Based Biotherapeutics to Pharmacologically Lower Asymmetric Dimethyl Arginine, thus Improving Postischemic Cardiac Function and Cardiomyocyte Mitochondrial Activity.

Young Lee, Jaipal Singh, Susan R Scott, Bradley Ellis, Pinar Zorlutuna, Meijing Wang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular pharmacology, 2022. 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
2.8field-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

7 citing papers in PubMed, 24 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

6 authors at 1 institution in 1 country.

Young LeeIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.).
Jaipal SinghIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.).
Susan R ScottIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.).
Bradley EllisIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.).
Pinar ZorlutunaIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.).
Meijing WangIndiana Center for Biomedical Innovation, Indianapolis, Indiana (Y.L., J.S.); Indiana University School of Medicine, Indianapolis, Indiana (J.S.); Department of Surgery, Indiana University, School of Medicine, Indianapolis, Indiana (S.R.S., M.W.); Bioengineering Graduate Program (B.E., P.Z.) and Aerospace and Mechanical Engineering Department (P.Z.), University of Notre Dame, Notre Dame, Indiana; and Vasculonics LLC, Indianapolis, Indiana (J.S.) meiwang@iupui.edu.
Indiana University – Purdue University Indianapolis · US

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Preclinical Development of a Novel Disease Modifying Therapy for Pulmonary Arterial HypertensionR33HL154135 · NHLBI · VASCULONICS, LLC · PI SINGH, JAIPAL · 2020 to 2021
$832k
A Potential DDAH-Biotherapeutic to Preserve Kidney Function in Cardiac Surgery PatientsR43DK125142 · NIDDK · VASCULONICS, LLC · PI SINGH, JAIPAL · 2020 to 2020
$235k
A Novel Disease Modifying Therapy for Progression of Pulmonary Arterial HypertensionR43HL149496 · NHLBI · VASCULONICS, LLC · PI SINGH, JAIPAL · 2019 to 2019
$218k
NCATS NIH HHS UL1 TR001108NHLBI NIH HHS R33 HL154135NHLBI NIH HHS R43 HL149496NIDDK NIH HHS R43 DK125142
6 · The paper itself

Abstract

High serum levels of asymmetric dimethyl arginine (ADMA) are associated with cardiovascular disease and mortality. Pharmacological agents to specifically lower ADMA and their potential impact on cardiovascular complications are not known. In this study, we aimed to investigate the effect of specific lowering of ADMA on myocardial response to ischemia-reperfusion injury (I/R) and direct effects on cardiomyocyte function. Effects of recombinant dimethylarginine dimethylaminohydrolase (rDDAH)-1 on I/R injury were determined using isolated mouse heart preparation. Respiration capacity and mitochondrial reactive oxygen species (ROS) generation were determined on mouse cardiomyocytes. Our results show that lowering ADMA by rDDAH-1 treatment resulted in improved recovery of cardiac function and reduction in myocardial infarct size in mouse heart response to I/R injury (control 22.24 ±4.60% versus rDDAH-1 15.90 ±4.23%,

Indexed as

Cardiovascular DiseasesInduced Pluripotent Stem CellsAmidohydrolasesAnimalsArginineEndothelial CellsHumansInterleukin-17MiceMitochondriaMyocytes, CardiacNitric OxideReactive Oxygen SpeciesAmidohydrolasesArgininedimethylargininaseInterleukin-17Nitric OxideReactive Oxygen Species

Identifiers

PMID35042831
PMCPMC11033929
OpenAlexW4205389351

What Socratic 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 Socratic graph.