Evidence map›Paper›PMID 25634538›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2015

Docetaxel Facilitates Endothelial Dysfunction through Oxidative Stress via Modulation of Protein Kinase C Beta: The Protective Effects of Sotrastaurin.

Ching-Hsia Hung, Shih-Hung Chan, Pei-Ming Chu, Kun-Ling Tsai

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  5. Radiation recall dermatitis in cancer patients previously undergoing radiotherapy: a scoping review.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
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  6. Cancer therapy and cachexia.The Journal of clinical investigation · 2025
    Review
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  9. Observational
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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

4 authors at 2 institutions in 1 country.

Ching-Hsia Hung*Department of Physical Therapy, National Cheng Kung University, Tainan, Taiwan, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan and Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Shih-Hung Chan*Department of Physical Therapy, National Cheng Kung University, Tainan, Taiwan, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan and Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Pei-Ming Chu*Department of Physical Therapy, National Cheng Kung University, Tainan, Taiwan, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan and Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Kun-Ling Tsai*Department of Physical Therapy, National Cheng Kung University, Tainan, Taiwan, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan and Department of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan kunlingtsai@mail.ncku.edu.tw.
China Medical University · TWNational Cheng Kung University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Docetaxel (DTX), a taxane drug, has widely been used as an anticancer or antiangiogenesis drug. However, DTX caused side effects, such as vessel damage and phlebitis, which may reduce its clinical therapeutic efficacy. The molecular mechanisms of DTX that cause endothelial dysfunction remain unclear. The aim of this study as to validate the probable mechanisms of DTX-induced endothelial dysfunction in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with DTX (2.5, 5, and 10nM) for 24 h to induce endothelial dysfunction. Stimulation with DTX reduced cell viability in a concentration- and time-dependent manner. DTX upregulated caspase-3 activity and TUNEL-positive cells. DTX treatment also increased PKCβ phosphorylation levels and NADPH oxidase activity, which resulted in ROS formation. However, all of these findings were reversed by PKCβ inhibition and NADPH oxidase repression. Finally, we demonstrated that sotrastaurin (AEB-071), a new PKCβ inhibitor, mitigated DTX-induced oxidative injury in endothelial cells. Our findings from this study provide a probable molecular mechanism of DTX-induced oxidative injury in endothelial cells and a new clinical and therapeutic approach for preventing DTX-mediated vessel injury.

Indexed as

Oxidative StressAntineoplastic Agents, PhytogenicDocetaxelEndothelium, VascularGlutathioneHumansHuman Umbilical Vein Endothelial CellsProtein Kinase C betaPyrrolesQuinazolinesReactive Oxygen SpeciesTaxoidsAntineoplastic Agents, PhytogenicDocetaxelGlutathioneProtein Kinase C betaPyrrolesQuinazolinesReactive Oxygen SpeciessotrastaurinTaxoidsdocetaxelNADPH oxidaseprotein kinase Csotrastaurin

Identifiers

PMID25634538
PMCPMC4833034
OpenAlexW2326882140

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.