Evidence map›Paper›PMID 22540532›Full record

ReviewAntioxidants & redox signaling2012

Reactive oxygen species and thiol redox signaling in the macrophage biology of atherosclerosis.

Sina Tavakoli, Reto Asmis

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

  1. Article
  2. Amelioration of Fe-Induced NaBiological trace element research · 2026
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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.

Sina TavakoliDepartment of Radiology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USA.
Reto Asmis

Funding

Role of Glutathione Reductase and Macrophage OncosisR01HL070963 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ASMIS, RETO H.R. · 2002 to 2010
$2.8M
RAPID BIOCHEMICAL KINETICS CORE FACILITYS10RR011313 · NCRR · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI ROSS, ELLIOTT M · 1997 to 1997
–
NCRR NIH HHS RR11313NHLBI NIH HHS HL-70963
6 · The paper itself

Abstract

significanceDespite the recent decline in the prevalence of cardiovascular diseases, atherosclerosis remains the leading cause of death in industrialized countries. Monocyte recruitment into the vessel wall is a rate-limiting step in atherogenesis. Death of macrophage-derived foam cells promotes lesion progression and the majority of acute complications of atherosclerotic disease (e.g., myocardial infarction) occur in lesions that are intensely infiltrated with monocyte-derived macrophages, underlining the critical roles monocytes and macrophages play in this complex chronic inflammatory disease. RECENT ADVANCES: A rapidly growing body of literature supports a critical role for reactive oxygen species (ROS) in the regulation of monocyte and macrophage (dys)function associated with atherogenesis and macrophage death in atherosclerotic plaque. CRITICAL ISSUES: In this review we highlight the important roles of NADHP oxidase 4 recently identified in monocytes and macrophages and the role of ROS and (thiol) redox signaling in different aspects of monocytes and macrophage biology associated with atherosclerosis. FUTURE DIRECTIONS: Studies aimed at identifying the intracellular targets of ROS involved in redox signaling in macrophages and at elucidating the redox signaling mechanisms that control differentiation, activation, polarization, and death of monocytes and macrophages may ultimately lead to the development of novel preventive and therapeutic strategies for atherosclerosis.

Indexed as

AnimalsAtherosclerosisHumansMacrophagesOxidation-ReductionReactive Oxygen SpeciesSignal TransductionReactive Oxygen Species

Identifiers

PMID22540532
PMCPMC3474194

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.