Evidence map›Paper›PMID 20078230›Full record

ReviewExpert opinion on biological therapy2010

Sarcoplasmic reticulum Ca(2+) ATPase as a therapeutic target for heart failure.

Larissa Lipskaia, Elie R Chemaly, Lahouaria Hadri, Anne-Marie Lompre, Roger J Hajjar

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on biological therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 187 citations in OpenAlex.

  1. Trial
  2. Review
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  6. Right Heart Diastology, Where Are We Now?Circulation research · 2026
    Review
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52 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Larissa LipskaiaCardiovascular Research Center, Mount Sinai School of Medicine, New York, NY 10029, USA.
Elie R Chemaly
Lahouaria Hadri
Anne-Marie Lompre
Roger J Hajjar
Icahn School of Medicine at Mount Sinai · USSorbonne Université · FRWeatherford College · US

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
Optical &MRI Imaging of Stem Cells in Diseased HeartsR01HL078691 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2004 to 2007
$2.6M
PICOT and Cardiac HypertrophyR01HL080498 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2006 to 2010
$2.2M
Targeting Calcium Cycling in Pre-Clinical Model CardiacR01HL083156 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2006 to 2010
$1.7M
ADENOVIRAL GENE TRANSFER OF CA++ ATPASE IN HEART FAILURER01HL057263 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER JOSEPH · 1999 to 2005
$1.7M
Gene Therapy with Cardiotropic Vectors for the Treatment of Heart FailureR01HL088434 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HAJJAR, ROGER J. · 2010 to 2013
$1.7M
K and Ca Channels in Cardiac Hypertrophy and FailureR01HL071763 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER J. · 2003 to 2006
$1.6M
Protein Phosphatase Inhibitor-1 and vascular smooth muscle cell functionK01HL103176 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HADRI, LAHOUARIA · 2010 to 2014
$674k
ADENOVIRAL GENE TRANSFER OF CA++ ATPASE IN HEART FAILURER29HL057263 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HAJJAR, ROGER JOSEPH · 1997 to 1998
–
NHLBI NIH HHS HL057263NHLBI NIH HHS HL071763NHLBI NIH HHS HL080498NHLBI NIH HHS HL083156NHLBI NIH HHS K01 HL103176NHLBI NIH HHS R01 HL057263NHLBI NIH HHS R01 HL071763NHLBI NIH HHS R01 HL078691NHLBI NIH HHS R01 HL080498NHLBI NIH HHS R01 HL083156NHLBI NIH HHS R01 HL088434NHLBI NIH HHS T32 HL007824
6 · The paper itself

Abstract

The cardiac isoform of the sarco/endoplasmic reticulum Ca(2+)ATPase (SERCA2a) plays a major role in controlling excitation/contraction coupling. In both experimental and clinical heart failure, SERCA2a expression is significantly reduced which leads to abnormal Ca(2+) handling and deficient contractility. A large number of studies in isolated cardiac myocytes and in small and large animal models of heart failure showed that restoring SERCA2a expression by gene transfer corrects the contractile abnormalities and improves energetics and electrical remodeling. Following a long line of investigation, a clinical trial is underway to restore SERCA2a expression in patients with heart failure using adeno-associated virus type 1. This review addresses the following issues regarding heart failure gene therapy: i) new insights on calcium regulation by SERCA2a; ii) SERCA2a as a gene therapy target in animal models of heart failure; iii) advances in the development of viral vectors and gene delivery; and iv) clinical trials on heart failure using SERCA2a. This review focuses on the new advances in SERCA2a- targeted gene therapy made in the last three years. In conclusion, SERCA2a is an important therapeutic target in various cardiovascular disorders. Ongoing clinical gene therapy trials will provide answers on its safety and applicability.

Indexed as

Genetic TherapyAnimalsHeart FailureHumansSarcoplasmic Reticulum Calcium-Transporting ATPasesSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID20078230
PMCPMC3001226
OpenAlexW2036920310

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.