Evidence map›Paper›PMID 26045778›Full record

ArticleInternational journal of clinical and experimental pathology2015

Upregulation of arginase activity contributes to intracellular ROS production induced by high glucose in H9c2 cells.

Lu Zhou, Chuan-Bo Sun, Chao Liu, Yue Fan, Hong-Yi Zhu, Xiao-Wei Wu, Liang Hu, Qing-Ping Li

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Roasted cashew (Heliyon · 2022
    Article
  6. Review
  7. Review
  8. Regulation of Ferroptosis by Amino Acid Metabolism in Cancer.International journal of biological sciences · 2022
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Serum exosomes mediate delivery of arginase 1 as a novel mechanism for endothelial dysfunction in diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. 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 at 1 institution in 1 country.

Lu ZhouDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Chuan-Bo SunDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Chao LiuDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Yue FanDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Hong-Yi ZhuDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Xiao-Wei WuDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Liang HuDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Qing-Ping LiDepartment of Pharmacology, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University Nanjing, P. R. China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arginase is upregulated in some tissues under diabetes states. Arginase can compete with nitroxide synthase (NOS) for the common substrate L-arginine and thus increases oxidative stress by NOS uncoupling. We want to analyze whether arginase is upregulated and contribute to oxidative stress in H9c2 cells during high glucose treatment. H9c2 cells were cultured in normal or high glucose DMEM. Arginase activity increased in parallel with increased cell death and oxidative stress. Arginase inhibitor N ω-hydroxy-nor-l-arginine (nor-NOHA) and NOS inhibitor N ω-nitro-l-arginine methyl ester (L-NAME) could reverse these effects. Despite of upregulated NOS activity, NO production was impaired which could be preserved by nor-NOHA, suggesting a decreased substrate availability of NOS due to increased arginase activity. L-arginine supplementation decreased superoxide production while it could not protect cells from death. Upregulated arginase activity in H9c2 treated with high glucose can cause NOS uncoupling and subsequently reactive oxygen species augmentation and cell death. These findings suggest that arginase will be a novel therapeutic target for treatment of diabetic cardiomyopathy.

Indexed as

Oxidative StressAnimalsApoptosisArginaseArginineCell LineDiabetic CardiomyopathiesEnzyme InhibitorsGlucoseMyocytes, CardiacNitric OxideNitric Oxide SynthaseRatsReactive Oxygen SpeciesSuperoxidesTime FactorsArginaseArginineEnzyme InhibitorsGlucoseNitric OxideNitric Oxide SynthaseReactive Oxygen SpeciesSuperoxidesArginasecardiomyocytediabetesNOS uncouplingoxidative stress

Identifiers

PMID26045778
PMCPMC4440087
OpenAlexW2402940147

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.