Evidence map›Paper›PMID 33328388›Full record

ArticleJCI insight2020

The negative feedback loop of NF-κB/miR-376b/NFKBIZ in septic acute kidney injury.

Zhiwen Liu, Chengyuan Tang, Liyu He, Danyi Yang, Juan Cai, Jiefu Zhu, Shaoqun Shu, Yuxue Liu, Lijun Yin, Guochun Chen and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
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  4. Emerging strategies to reduce the side effects of CAR-T cell therapy: focusing on gene editing and nanotechnology.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  5. NAT10-mediated acCellular & molecular biology letters · 2026
    Article
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  11. Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Proteome characterization of liver-kidney comorbidity after microbial sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

13 authors at 2 institutions in 2 countries.

Zhiwen LiuDepartment of Nephrology and.
Chengyuan TangDepartment of Nephrology and.
Liyu HeDepartment of Nephrology and.
Danyi YangDepartment of Nephrology and.
Juan CaiDepartment of Nephrology and.
Jiefu ZhuDepartment of Nephrology and.
Shaoqun ShuDepartment of Nephrology and.
Yuxue LiuDepartment of Nephrology and.
Lijun YinDepartment of Nephrology and.
Guochun ChenDepartment of Nephrology and.
Yu LiuDepartment of Nephrology and.
Dongshan ZhangDepartment of Nephrology and.
Zheng DongDepartment of Nephrology and.
Augusta University · USCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is the leading cause of acute kidney injury (AKI). However, the pathogenesis of septic AKI remains largely unclear. Here, we demonstrate a significant decrease of microRNA-376b (miR-376b) in renal tubular cells in mice with septic AKI. Urinary miR-376b in these mice was also dramatically decreased. Patients with sepsis with AKI also had significantly lower urinary miR-376b than patients with sepsis without AKI, supporting its diagnostic value for septic AKI. LPS treatment of renal tubular cells led to the activation of NF-κB, and inhibition of NF-κB prevented a decrease of miR-376b. ChIP assay further verified NF-κB binding to the miR-376b gene promoter upon LPS treatment. Functionally, miR-376b mimics exaggerated tubular cell death, kidney injury, and intrarenal production of inflammatory cytokines, while inhibiting miR-376b afforded protective effects in septic mice. Interestingly, miR-376b suppressed the expression of NF-κB inhibitor ζ (NFKBIZ) in both in vitro and in vivo models of septic AKI. Luciferase microRNA target reporter assay further verified NFKBIZ as a direct target of miR-376b. Collectively, these results illustrate the NF-κB/miR-376b/NFKBIZ negative feedback loop that regulates intrarenal inflammation and tubular damage in septic AKI. Moreover, urinary miR-376b is a potential biomarker for the diagnosis of AKI in patients with sepsis.

Indexed as

Acute Kidney InjuryAdaptor Proteins, Signal TransducingAnimalsApoptosisFeedback, PhysiologicalInflammationKidneyMaleMiceMice, Inbred C57BLMicroRNAsNF-kappa BSepsisSignal TransductionAdaptor Proteins, Signal TransducingMicroRNAsMIRN376b microRNA, mouseMIRN376C microRNA, humanNF-kappa BNFKBIZ protein, humanNfkbiz protein, mouseDiagnosticsEpigeneticsNephrologyNF-kappaB

Identifiers

PMID33328388
PMCPMC7819752
OpenAlexW3113184077

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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.