Evidence map›Paper›PMID 31861356›Full record

ReviewCells2019

Metabolic Reprogramming in Mitochondria of Myeloid Cells.

Hao Zuo, Yihong Wan

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
  2. Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  18. Molecular therapy. Nucleic acids · 2022
    Article
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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.

Hao ZuoDepartment of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0002-8812-7385
Yihong WanDepartment of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
The University of Texas Southwestern Medical Center · US

Funding

Context-Dependent Effects of PARP Inhibitors on Breast Cancer Bone MetastasisR01CA229487 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KRAUS, WILLIAM LEE · 2018 to 2023
$1.8M
Novel Mechanisms of Cancer Bone MetastasisR01CA236802 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WAN, YIHONG · 2019 to 2020
$741k
NCI NIH HHS R01 CA229487NCI NIH HHS R01 CA236802
6 · The paper itself

Abstract

The myeloid lineage consists of multiple immune cell types, such as macrophages, monocytes, and dendritic cells. It actively participates in both innate and adaptive immunity. In response to pro- or anti-inflammatory signals, these cells undergo distinct programmed metabolic changes especially in mitochondria. Pro-inflammatory signals induce not only a simple shift from oxidative phosphorylation to glycolysis, but also complicated metabolic alterations during the early and tolerant stages in myeloid cells. In mitochondria, a broken Krebs cycle leads to the accumulation of two metabolites, citrate and succinate, both of which trigger pro-inflammatory responses of myeloid cells. A deficient electron transport chain induces pro-inflammatory responses in the resting myeloid cells while it suppresses these responses in the polarized cells during inflammation. The metabolic reprogramming in mitochondria is also associated with altered mitochondrial morphology. On the other hand, intact oxidative phosphorylation is required for the anti-inflammatory functions of myeloid cells. Fatty acid synthesis is essential for the pro-inflammatory effect and glutamine metabolism in mitochondria exhibits the anti-inflammatory effect. A few aspects of metabolic reprogramming remain uncertain, for example, glycolysis and fatty acid oxidation in anti-inflammation. Overall, metabolic reprogramming is an important element of immune responses in myeloid cells.

Indexed as

Adaptive ImmunityCitric Acid CycleGlycolysisHumansImmunity, InnateMitochondriaMyeloid CellsOxidative Phosphorylationelectron transport chainglycolysisinflammationKrebs cyclemacrophagesmetabolismmitochondriamyeloid cellsoxidative phosphorylation

Identifiers

PMID31861356
PMCPMC7017304
OpenAlexW2994824513

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.