Evidence map›Paper›PMID 26423352›Full record

ArticleScientific reports2015

The protein kinase 2 inhibitor tetrabromobenzotriazole protects against renal ischemia reperfusion injury.

Sun-O Ka, Hong Pil Hwang, Jong-Hwa Jang, In Hyuk Bang, Ui-Jin Bae, Hee Chul Yu, Baik Hwan Cho, Byung-Hyun Park

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
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  8. Casein Kinase 2 Signaling in White Matter Stroke.Frontiers in molecular biosciences · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Article
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  14. Article
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  17. Exploring the CK2 Paradox: Restless, Dangerous, Dispensable.Pharmaceuticals (Basel, Switzerland) · 2017
    Review
  18. 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

8 authors.

Sun-O KaDepartment of Biochemistry, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Hong Pil HwangDepartment of Surgery and Research Institute of Clinical Medicine, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Jong-Hwa JangDepartment of Dental Hygiene, Hanseo University, 46 Hanseo 1 ro, Seasan, Chungnam 31962, Republic of Korea.
In Hyuk BangDepartment of Biochemistry, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Ui-Jin BaeDepartment of Biochemistry, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Hee Chul YuDepartment of Surgery and Research Institute of Clinical Medicine, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Baik Hwan ChoDepartment of Surgery and Research Institute of Clinical Medicine, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.
Byung-Hyun ParkDepartment of Biochemistry, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk 54896, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase 2 (CK2) activation was reported to enhance reactive oxygen species production and activate the nuclear factor κB (NF-κB) pathway. Because oxidative stress and inflammation are critical events for tissue destruction during ischemia reperfusion (I/R), we sought to determine whether CK2 was important in the renal response to I/R. Mice underwent 25 min of renal ischemia and were then reperfused. We confirmed an increased expression of CK2α during the reperfusion period, while expression of CK2β remained consistent. We administered tetrabromobenzotriazole (TBBt), a selective CK2α inhibitor before inducing I/R injury. Mice subjected to I/R injury showed typical patterns of acute kidney injury; blood urea nitrogen and serum creatinine levels, tubular necrosis and apoptosis, inflammatory cell infiltration and proinflammatory cytokine production, and oxidative stress were markedly increased when compared to sham mice. However, pretreatment with TBBt abolished these changes and improved renal function and architecture. Similar renoprotective effects of CK2α inhibition were observed for emodin. Renoprotective effects of CK2α inhibition were associated with suppression of NF-κB and mitogen activated protein kinase (MAPK) pathways. Taken together, these results suggest that CK2α mediates proapoptotic and proinflammatory signaling, thus the CK2α inhibitor may be used to prevent renal I/R injuries observed in clinical settings.

Indexed as

AnimalsApoptosisCasein Kinase IIExtracellular Signal-Regulated MAP KinasesGene ExpressionInflammation MediatorsKidney DiseasesMaleMiceMitogen-Activated Protein KinasesNF-kappa BOxidative Stressp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReperfusion InjurySignal TransductionCasein Kinase IIExtracellular Signal-Regulated MAP KinasesInflammation MediatorsMitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesProtein Kinase Inhibitors

Identifiers

PMID26423352
PMCPMC4589787

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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.