Evidence map›Paper›PMID 27960539›Full record

ArticleAntioxidants & redox signaling2017

C-X-C Chemokine Receptor Type 4 Plays a Crucial Role in Mediating Oxidative Stress-Induced Podocyte Injury.

Hongyan Mo, Qinyu Wu, Jinhua Miao, Congwei Luo, Xue Hong, Yongping Wang, Lan Tang, Fan Fan Hou, Youhua Liu, Lili Zhou

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 3 institutions in 2 countries.

Hongyan Mo1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Qinyu Wu1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Jinhua Miao1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Congwei Luo1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Xue Hong1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Yongping Wang1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Lan Tang2 Guangdong Provincial Key Laboratory of New Drug Screening, Department of Biopharmaceutics, School of Pharmaceutical Sciences, Southern Medical University , Guangzhou, China .
Fan Fan Hou1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Youhua Liu1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Lili Zhou1 State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Division of Nephrology, Nanfang Hospital, Southern Medical University , Guangzhou, China .
Nanfang Hospital · CNGuangdong Pharmaceutical University · CNUniversity of Pittsburgh · US

Funding

Central role of fibroblasts in kidney repair and disease after AKIR01DK106049 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LIU, YOUHUA · 2015 to 2018
$1.4M
NIDDK NIH HHS R01 DK106049
6 · The paper itself

Abstract

aimsOxidative stress plays a role in mediating podocyte injury and proteinuria. However, the underlying mechanism remains poorly understood. In this study, we investigated the potential role of C-X-C chemokine receptor type 4 (CXCR4), the receptor for stromal cell-derived factor 1α (SDF-1α), in mediating oxidative stress-induced podocyte injury.

resultsIn mouse model of adriamycin nephropathy (ADR), CXCR4 expression was significantly induced in podocytes as early as 3 days. This was accompanied by an increased upregulation of oxidative stress in podocyte, as demonstrated by malondialdehyde assay, nitrotyrosine staining and secretion of 8-hydroxy-2'-deoxyguanosine in urine, and induction of NOX2 and NOX4, major subunits of NADPH oxidase. CXCR4 was also induced in human kidney biopsies with proteinuric kidney diseases and colocalized with advanced oxidation protein products (AOPPs), an established oxidative stress trigger. Using cultured podocytes and mouse model, we found that AOPPs induced significant loss of podocyte marker Wilms tumor 1 (WT1), nephrin, and podocalyxin, accompanied by upregulation of desmin both in vitro and in vivo. Furthermore, AOPPs worsened proteinuria and aggravated glomerulosclerosis in ADR. These effects were associated with marked activation of SDF-1α/CXCR4 axis in podocytes. Administration of AMD3100, a specific inhibitor of CXCR4, reduced proteinuria and ameliorated podocyte dysfunction and renal fibrosis triggered by AOPPs in mice. In glomerular miniorgan culture, AOPPs also induced CXCR4 expression and downregulated nephrin and WT1. Innovation and Conclusion: These results suggest that chemokine receptor CXCR4 plays a crucial role in mediating oxidative stress-induced podocyte injury, proteinuria, and renal fibrosis. CXCR4 could be a new target for mitigating podocyte injury, proteinuria, and glomerular sclerosis in proteinuric chronic kidney disease. Antioxid. Redox Signal. 27, 345-362.

Indexed as

Advanced Oxidation Protein ProductsAnimalsBenzylaminesBiopsyCells, CulturedChemical and Drug Induced Liver InjuryCyclamsDisease Models, AnimalDoxorubicinHeterocyclic CompoundsHumansMiceOxidative StressPodocytesProteinuriaReceptors, CXCR4Advanced Oxidation Protein ProductsBenzylaminesCXCR4 protein, humanCyclamsDoxorubicinHeterocyclic CompoundsplerixaforReceptors, CXCR4CXCR4oxidative stresspodocyte injury

Identifiers

PMID27960539
PMCPMC6435352
OpenAlexW2599348491

What OpenQuestion holds

Textmetadata
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.