Evidence map›Paper›PMID 15031632›Full record

ReviewJournal of clinical immunology2003

Mechanisms of apoptosis in the heart.

Asa B Gustafsson, Roberta A Gottlieb

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

56 citing papers in PubMed, 134 citations in OpenAlex.

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  15. Effects of Four Compounds fromBioMed research international · 2019
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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

2 authors at 1 institution in 1 country.

Asa B GustafssonDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
Roberta A Gottlieb
Scripps Research Institute · US

Funding

Rescue and Role of Complex I in myocardial ischemic injuryR01HL060590 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GOTTLIEB, ROBERTA A. · 1998 to 2011
$3.6M
SUPPLEMENT TO INVESTIGATIVE HEMATOLOGYT32DK007022 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI SOLOMON, DANIEL RENEE · 1986 to 2009
$2.3M
NHLBI NIH HHS HL 60590NHLBI NIH HHS HL 6/5/8NIDDK NIH HHS DK 07022
6 · The paper itself

Abstract

Apoptosis is a complex and highly regulated form of cell death, and believed to contribute to the continuous decline of ventricular function in heart failure. Apoptotic cell death is observed in a variety of cardiovascular diseases, including myocardial infarction, ischemia-reperfusion injury, end-stage heart failure, arrhythmias, and adriamycin cardiomyopathy. There are several pathways leading to programmed cell death. Apoptosis can be initiated by extracellular or intracellular stimuli, leading to the activation of caspases and subsequent cell death. A better understanding of the process of apoptosis in the heart is clearly important as it may lead to the identification of novel therapies for cardiovascular disease. This review is focused on the basic cellular mechanisms of apoptosis, as well as our current understanding of this process in the heart.

Indexed as

AnimalsApoptosisCalciumCaspasesHumansMAP Kinase Signaling SystemMitochondria, HeartMyocardiumProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSignal TransductionCalciumCaspasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen Species

Identifiers

PMID15031632
OpenAlexW2081596112

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.