Evidence map›Paper›PMID 19583492›Full record

ReviewAntioxidants & redox signaling2009

Redox regulation of cell survival by the thioredoxin superfamily: an implication of redox gene therapy in the heart.

Md Kaimul Ahsan, Istvan Lekli, Diptarka Ray, Junji Yodoi, Dipak K Das

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 134 citations in OpenAlex.

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  2. ROS-Balancing MXene/MoSeSmall (Weinheim an der Bergstrasse, Germany) · 2026
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  5. A selenomethionine deficient, high-fructose diet does not lead to cardiometabolic disorder in the selenocysteine lyase knockout mice.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
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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

5 authors at 2 institutions in 2 countries.

Md Kaimul AhsanCardiovascular Research Center, Department of Surgery, School of Medicine, University of Connecticut Health Center , Farmington, CT 06030-1110, USA. ddas@neuron.uchc.edu
Istvan Lekli
Diptarka Ray
Junji Yodoi
Dipak K Das
UConn Health · USKyoto University · JP

Funding

PHOSPHOLIPIDS IN MYOCARDIAL REPERFUSION INJURYR01HL034360 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DAS, DIPAK K · 1987 to 2009
$2.8M
MYOCARDIAL PRESERVATION DURING ISCHEMIC ARRESTR01HL022559 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DAS, DIPAK K · 1985 to 2008
$2.7M
SUPEROXIDE RADICALS IN REPERFUSION INJURYR01HL033889 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DAS, DIPAK K · 1986 to 1988
–
NHLBI NIH HHS HL 22559NHLBI NIH HHS HL 33889NHLBI NIH HHS HL34360
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are the key mediators of pathogenesis in cardiovascular diseases. Members of the thioredoxin superfamily take an active part in scavenging reactive oxygen species, thus playing an essential role in maintaining the intracellular redox status. The alteration in the expression levels of thioredoxin family members and related molecules constitute effective biomarkers in various diseases, including cardiovascular complications that involve oxidative stress. Thioredoxin, glutaredoxin, peroxiredoxin, and glutathione peroxidase, along with their isoforms, are involved in interaction with the members of metabolic and signaling pathways, thus making them attractive targets for clinical intervention. Studies with cells and transgenic animals have supported this notion and raised the hope for possible gene therapy as modern genetic medicine. Of all the molecules, thioredoxins, glutaredoxins, and peroxiredoxins are emphasized, because a growing body of evidence reveals their essential and regulatory role in several steps of redox regulation. In this review, we discuss some pertinent observations regarding their distribution, structure, functions, and interactions with the several survival- and death-signaling pathways, especially in the myocardium.

Indexed as

Genetic TherapyOxidation-ReductionAnimalsCell SurvivalGlutaredoxinsHumansModels, BiologicalMyocardiumPeroxiredoxinsSignal TransductionThioredoxinsGlutaredoxinsPeroxiredoxinsThioredoxins

Identifiers

PMID19583492
PMCPMC2821134
OpenAlexW1963661977

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.