Evidence map›Paper›PMID 28739140›Full record

ArticleKidney international2017

The IL-4 receptor α has a critical role in bone marrow-derived fibroblast activation and renal fibrosis.

Hua Liang, Zhengmao Zhang, Jingyin Yan, Yuguo Wang, Zhaoyong Hu, William E Mitch, Yanlin Wang

Abstract read
In one paragraph

Article in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Macrophage RNA polymerase II subunit 5-mediating protein deficiency exacerbates kidney inflammation and fibrosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
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  16. Article
  17. JMJD3 ablation in myeloid cells confers renoprotection in mice with DOCA/salt-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  18. Article
  19. Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023
    Review
  20. Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism.Frontiers in cell and developmental biology · 2023
    Review
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

7 authors at 3 institutions in 2 countries.

Hua LiangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA; Department of Anesthesiology, Affiliated Foshan Hospital of Sun Yat-Sen University, Foshan, China.
Zhengmao ZhangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Jingyin YanSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Yuguo WangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Zhaoyong HuSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
William E MitchSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Yanlin WangSelzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA; Center for Translational Research on Inflammatory Diseases and Renal Section, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA. Electronic address: yanlinw@bcm.edu.
Baylor College of Medicine · USMichael E. DeBakey VA Medical Center · USSun Yat-sen University · CN

Funding

PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
Cellular and Molecular Mechanisms of Renal FibrosisR01DK095835 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WANG, YANLIN · 2012 to 2021
$3.2M
Mechanisms of Protein-Energy-Wasting in Chronic Kidney DiseaseR01AR063686 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI HU, ZHAOYONG · 2013 to 2017
$1.7M
Research Training in Renal DiseasesT32DK062706 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2003 to 2013
$1.5M
Targeting histone deacetylase 3 for chronic kidney diseaseI01BX002650 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI YANLIN WANG · 2016 to 2026
–
BLRD VA I01 BX002650NIAMS NIH HHS R01 AR063686NIDDK NIH HHS R01 DK095835NIDDK NIH HHS R37 DK037175NIDDK NIH HHS T32 DK062706
6 · The paper itself

Abstract

Renal fibrosis is a common pathway leading to the progression of chronic kidney disease, and bone marrow-derived fibroblasts contribute significantly to the development of renal fibrosis. However, the signaling mechanisms underlying the activation of these fibroblasts are not completely understood. Here, we examined the role of IL-4 receptor α (IL-4Rα) in the activation of myeloid fibroblasts in two experimental models of renal fibrosis. Compared with wild-type mice, IL-4Rα knockout mice accumulated fewer bone marrow-derived fibroblasts and myofibroblasts in their kidneys. IL-4Rα deficiency suppressed the expression of α-smooth muscle actin, extracellular matrix proteins and the development of renal fibrosis. Furthermore, IL-4Rα deficiency inhibited the activation of signal transducer and activator of transcription 6 (STAT6) in the kidney. Moreover, wild-type mice engrafted with bone marrow cells from IL-4Rα knockout mice exhibited fewer myeloid fibroblasts in the kidney and displayed less severe renal fibrosis following ureteral obstructive injury compared with wild-type mice engrafted with wild-type bone marrow cells. In vitro, IL-4 activated STAT6 and stimulated expression of α-smooth muscle actin and fibronectin in mouse bone marrow monocytes. This was abolished in the absence of IL-4Rα. Thus, IL-4Rα plays an important role in bone marrow-derived fibroblast activation, resulting in extracellular matrix protein production and fibrosis development. Hence, the IL-4Rα/STAT6 signaling pathway may serve as a novel therapeutic target for chronic kidney disease.

Indexed as

ActinsAnimalsBone Marrow CellsBone Marrow TransplantationDisease Models, AnimalDisease ProgressionExtracellular Matrix ProteinsFibroblastsFibrosisFolic AcidHumansInterleukin-4 Receptor alpha SubunitKidneyMaleMiceMice, Inbred BALB CActinsalpha-smooth muscle actin, mouseExtracellular Matrix ProteinsFolic AcidIl4ra protein, mouseInterleukin-4 Receptor alpha SubunitReceptors, Cell SurfaceStat6 protein, mouseSTAT6 Transcription Factorchronic kidney diseasecytokinesextracellular matrixfibroblastfibrosis

Identifiers

PMID28739140
PMCPMC5696054
OpenAlexW2736499210

What OpenQuestion holds

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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.