Evidence map›Paper›PMID 30666533›Full record

ReviewHeart failure reviews2019

Experimental models of cardiac physiology and pathology.

Jae Gyun Oh, Changwon Kho, Roger J Hajjar, Kiyotake Ishikawa

Abstract readReview
In one paragraph

Review in Heart failure reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
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  17. Article
  18. Progression of infarct-mediated arrhythmogenesis in a rodent model of heart failure.American journal of physiology. Heart and circulatory physiology · 2021
    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

4 authors.

Jae Gyun OhIcahn School of Medicine at Mount Sinai, New York, USA.
Changwon KhoIcahn School of Medicine at Mount Sinai, New York, USA.
Roger J HajjarIcahn School of Medicine at Mount Sinai, New York, USA.
Kiyotake IshikawaIcahn School of Medicine at Mount Sinai, New York, USA. kiyotake.ishikawa@mssm.edu.ORCID 0000-0002-8287-3483

Funding

TRAINING PROGRAM IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007824 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GELB, BRUCE D · 1995 to 2022
$8.6M
Percutaneous Left Ventricular Unloading for Cardiogenic Shock: Beyond Acute Hemodynamic SupportR01HL139963 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Kiyotake Ishikawa · 2018 to 2026
$4.9M
SUMO1 and SERCA2a FunctionR01HL117505 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WEBER, THOMAS · 2013 to 2020
$3.4M
Anti-AAV Antibodies as an Obstacle to Cardiac AAV Gene TherapyR01HL131404 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WEBER, THOMAS · 2016 to 2019
$3.3M
Calcium Pump Activators for Heart Failure TherapyR01HL129814 · NHLBI · UNIVERSITY OF MINNESOTA · PI THOMAS, DAVID D · 2015 to 2018
$3.2M
Targeting Abnormal Calcium Cycling Using Novel Gene Therapy VectorsR01HL119046 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI AKAR, FADI GABRIEL, HAJJAR, ROGER J. · 2014 to 2017
$2.9M
Treating Ventricle and Valve: New Synergies for Ischemic LV Remodeling with MRR01HL128099 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AKAR, FADI GABRIEL, LEVINE, ROBERT A · 2016 to 2019
$2.8M
The Role of Post-translational Acetylation in SERCA2a-related Cardiac DysfunctionR00HL116645 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KHO, CHANGWON · 2015 to 2017
$747k
The role of post-translational acetylation in SERCA2a-related cardiac dysfunctionK99HL116645 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KHO, CHANGWON · 2013 to 2014
$260k
aha 17POST33410877aha 17SDG33410873American Heart Association-American Stroke Association 17POST33410877leducq NANational Institutes of Health (US) HL139963NHLBI NIH HHS HL116645NHLBI NIH HHS R00 HL116645NHLBI NIH HHS R01 HL117505NHLBI NIH HHS R01 HL119046NHLBI NIH HHS R01 HL128099NHLBI NIH HHS R01 HL129814NHLBI NIH HHS R01 HL131404NHLBI NIH HHS R01 HL139963NHLBI NIH HHS T32 HL007824NIH HHS HL007824NIH HHS HL117505NIH HHS HL119046NIH HHS HL128099NIH HHS HL129814NIH HHS HL131404
6 · The paper itself

Abstract

Experimental models of cardiac disease play a key role in understanding the pathophysiology of the disease and developing new therapies. The features of the experimental models should reflect the clinical phenotype, which can have a wide spectrum of underlying mechanisms. We review characteristics of commonly used experimental models of cardiac physiology and pathophysiology in all translational steps including in vitro, small animal, and large animal models. Understanding their characteristics and relevance to clinical disease is the key for successful translation to effective therapies.

Indexed as

Models, BiologicalAnimalsCell LineDisease Models, AnimalHeartHeart DiseasesHumansIn Vitro TechniquesMyocytes, CardiacTissue EngineeringIschemicNeonatal cardiomyocytesNon-ischemicPressure overloadPrimary cardiomyocytesVolume overload

Identifiers

PMID30666533
PMCPMC6561792

What Socratic 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 Socratic graph.