Evidence map›Paper›PMID 34278465›Full record

ArticleInternational journal of molecular medicine2021

Bruton's tyrosine kinase regulates macrophage‑induced inflammation in the diabetic kidney via NLRP3 inflammasome activation.

Jing Zhao, Juan Chen, Yuan-Yuan Li, Ling-Ling Xia, Yong-Gui Wu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. 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
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  6. Using digital pathology to analyze the murine cerebrovasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. UnveilingJournal of inflammation research · 2023
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. 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

5 authors at 1 institution in 1 country.

Jing ZhaoDepartment of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Juan ChenDepartment of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Yuan-Yuan LiDepartment of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Ling-Ling XiaDepartment of Infectious Diseases, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Yong-Gui WuDepartment of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been previously reported that macrophages may be involved in diabetic nephropathy (DN) development. Furthermore, Bruton's tyrosine kinase (BTK) may participate in macrophage activation and lead to the release of inflammatory mediators. The main aim of the present study was to analyze the association between renal BTK expression and clinical indicators. Moreover, BTK knockout mice were used to establish a diabetic model for further research. The results demonstrated that BTK was activated in the kidneys of patients with DN and was associated with the progression of proteinuria, creatinine levels, estimated glomerular filtration rate and pathological changes in the kidneys of patients with DN. Furthermore, BTK knockout was observed to reduce urinary protein excretion, alleviate renal injury and decrease renal inflammation in diabetic mice. This protection may be attributed to BTK‑induced suppression of the activation of the Nod‑like receptor (NLR) family pyrin domain containing 3 inflammasome. Collectively, it has been demonstrated in the present study that BTK may be a potential target for DN treatment.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEnzyme ActivationHumansInflammasomesInflammationMacrophagesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinAgammaglobulinaemia Tyrosine KinaseBtk protein, mouseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseBruton's tyrosine kinasediabetic nephropathyinflammationmacrophageNod‑like receptor family pyrin domain containing 3

Identifiers

PMID34278465
PMCPMC8354311
OpenAlexW3184125012

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.