Evidence map›Paper›PMID 37629049›Full record

ArticleInternational journal of molecular sciences2023

A Model of iPSC-Derived Macrophages with

Olga Sheveleva, Elena Protasova, Tatiana Nenasheva, Nina Butorina, Victoria Melnikova, Tatiana Gerasimova, Olga Sakovnich, Alexander Kurinov, Elena Grigor'eva, Sergey Medvedev and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

11 authors at 2 institutions in 1 country.

Olga ShevelevaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.
Elena ProtasovaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.ORCID 0000-0002-3457-4526
Tatiana NenashevaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.ORCID 0000-0002-1669-5244
Nina ButorinaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.
Victoria MelnikovaLaboratory of Comparative Developmental Physiology, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.ORCID 0000-0003-2851-7039
Tatiana GerasimovaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.ORCID 0000-0002-3858-4561
Olga SakovnichLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.
Alexander KurinovLaboratory of Regeneration Problems, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.
Elena Grigor'evaLaboratory of Developmental Epigenetics, Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, Lavrentyev Ave., 10, 630090 Novosibirsk, Russia.
Sergey MedvedevLaboratory of Developmental Epigenetics, Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, Lavrentyev Ave., 10, 630090 Novosibirsk, Russia.ORCID 0000-0002-1520-5549
Irina LyadovaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of Russian Academy of Sciences, Vavilova Str., 26, 119334 Moscow, Russia.
Koltzov Institute of Developmental Biology · RUInstitute of Cytology and Genetics · RU

Funding

Ministry of Science and Higher Education of the Russian Federation 0088-2021-0016Ministry of Science and Higher Education of the Russian Federation 075-15-2020-773
6 · The paper itself

Abstract

Macrophages play a crucial role in the development and control of inflammation. Understanding the mechanisms balancing macrophage inflammatory activity is important to develop new strategies for treating inflammation-related diseases. TNF-α-induced protein 3 (TNFAIP3, A20) is a negative regulator of intracellular inflammatory cascades; its deficiency induces hyper-inflammatory reactions. Whether A20 overexpression can dampen macrophage inflammatory response remains unclear. Here, we generated human-induced pluripotent stem cells with tetracycline-inducible A20 expression and differentiated them into macrophages (A20-iMacs). A20-iMacs displayed morphology, phenotype, and phagocytic activity typical of macrophages, and they displayed upregulated A20 expression in response to doxycycline. A20 overexpression dampened the A20-iMac response to TNF-α, as shown by a decreased expression of

Indexed as

Induced Pluripotent Stem CellsTumor Necrosis Factor-alphaHumansInflammationMacrophagesTumor Necrosis Factor alpha-Induced Protein 3TNFAIP3 protein, humanTumor Necrosis Factor-alphaTumor Necrosis Factor alpha-Induced Protein 3A20doxycycline-inducible gene expressioninduced pluripotent stem cellsinflammatory responsemacrophages derived from induced pluripotent stem cellsTNFAIP3

Identifiers

PMID37629049
PMCPMC10454046
OpenAlexW4385877492

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.