Evidence map›Paper›PMID 33114647›Full record

ReviewMetabolites2020

Nitric Oxide in Macrophage Immunometabolism: Hiding in Plain Sight.

Erika M Palmieri, Christopher McGinity, David A Wink, Daniel W McVicar

Open access · goldAbstract readReview
In one paragraph

Review in Metabolites, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
6.7field-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

115 citing papers in PubMed, 217 citations in OpenAlex.

  1. Review
  2. Ketotifen attenuates paraquat-induced nephrotoxicity in miceResearch in pharmaceutical sciences · 2026
    Article
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55 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

4 authors at 1 institution in 1 country.

Erika M PalmieriLaboratory of Cancer ImmunoMetabolism, National Cancer Institute, Frederick, MD 21702, USA.ORCID 0000-0002-4237-5324
Christopher McGinityLaboratory of Cancer ImmunoMetabolism, National Cancer Institute, Frederick, MD 21702, USA.
David A WinkLaboratory of Cancer ImmunoMetabolism, National Cancer Institute, Frederick, MD 21702, USA.
Daniel W McVicarLaboratory of Cancer ImmunoMetabolism, National Cancer Institute, Frederick, MD 21702, USA.
National Cancer Institute · US

Funding

Signal Transduction of Paired Inhibitory Receptors of NK Cells and MacrophagesZIABC010300 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MCVICAR, DANIEL W. · 2009 to 2025
$24.6M
Properties of redox modified NSAIDs in cancer prevention and treatmentZIABC010899 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$6.7M
NCI NIH HHS ZIA BC 010300NCI NIH HHS ZIA BC 010899
6 · The paper itself

Abstract

Nitric Oxide (NO) is a soluble endogenous gas with various biological functions like signaling, and working as an effector molecule or metabolic regulator. In response to inflammatory signals, immune myeloid cells, like macrophages, increase production of cytokines and NO, which is important for pathogen killing. Under these proinflammatory circumstances, called "M1", macrophages undergo a series of metabolic changes including rewiring of their tricarboxylic acid (TCA) cycle. Here, we review findings indicating that NO, through its interaction with heme and non-heme metal containing proteins, together with components of the electron transport chain, functions not only as a regulator of cell respiration, but also a modulator of intracellular cell metabolism. Moreover, diverse effects of NO and NO-derived reactive nitrogen species (RNS) involve precise interactions with different targets depending on concentration, temporal, and spatial restrictions. Although the role of NO in macrophage reprogramming has been in evidence for some time, current models have largely minimized its importance. It has, therefore, been hiding in plain sight. A review of the chemical properties of NO, past biochemical studies, and recent publications, necessitates that mechanisms of macrophage TCA reprogramming during stimulation must be re-imagined and re-interpreted as mechanistic results of NO exposure. The revised model of metabolic rewiring we describe here incorporates many early findings regarding NO biochemistry and brings NO out of hiding and to the forefront of macrophages immunometabolism.

Indexed as

macrophagemetabolic reprogrammingnitric oxide

Identifiers

PMID33114647
PMCPMC7693038
OpenAlexW3096340664

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.