Evidence map›Paper›PMID 38201227›Full record

ArticleCells2023

NLRX1 Prevents M2 Macrophage Polarization and Excessive Renal Fibrosis in Chronic Obstructive Nephropathy.

Ye Liu, Lotte Kors, Loes M Butter, Geurt Stokman, Nike Claessen, Coert J Zuurbier, Stephen E Girardin, Jaklien C Leemans, Sandrine Florquin, Alessandra Tammaro

Abstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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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

10 authors.

Ye LiuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Lotte KorsDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Loes M ButterDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Geurt StokmanDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.ORCID 0000-0002-3280-6311
Nike ClaessenDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Coert J ZuurbierDepartment of Anesthesiology, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.ORCID 0000-0001-8361-2448
Stephen E GirardinDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A1, Canada.
Jaklien C LeemansDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Sandrine FlorquinDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.
Alessandra TammaroDepartment of Pathology, Amsterdam Infection & Immunity, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands.ORCID 0000-0003-3128-5259

Funding

Netherlands Organisation for Health Research and Development 457002002
6 · The paper itself

Abstract

backgroundChronic kidney disease often leads to kidney dysfunction due to renal fibrosis, regardless of the initial cause of kidney damage. Macrophages are crucial players in the progression of renal fibrosis as they stimulate inflammation, activate fibroblasts, and contribute to extracellular matrix deposition, influenced by their metabolic state. Nucleotide-binding domain and LRR-containing protein X (NLRX1) is an innate immune receptor independent of inflammasomes and is found in mitochondria, and it plays a role in immune responses and cell metabolism. The specific impact of NLRX1 on macrophages and its involvement in renal fibrosis is not fully understood.

methodsTo explore the specific role of NLRX1 in macrophages, bone-marrow-derived macrophages (BMDMs) extracted from wild-type (WT) and NLRX1 knockout (KO) mice were stimulated with pro-inflammatory and pro-fibrotic factors to induce M1 and M2 polarization in vitro. The expression levels of macrophage polarization markers (

resultsCompared to the WT group, an increased gene expression of M2 markers-including

conclusionsOur findings highlight the unique role of NLRX1 in regulating the metabolism and function of macrophages, ultimately protecting against excessive renal injury and fibrosis in UUO.

Indexed as

Renal Insufficiency, ChronicAnimalsFibrosisGenes, RegulatorMacrophagesMiceMitochondrial ProteinsTransforming Growth Factor betaMitochondrial ProteinsNLRX1 protein, mouseTransforming Growth Factor betamacrophage polarizationNLRX1OXPHOSrenal fibrosis

Identifiers

PMID38201227
PMCPMC10778504

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Registered trials

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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.