MétaCan
Menu
Back to cohort

RAC1 SIGNALLING MEDIATES DOXORUBICIN-INDUCED CARDIOTOXICITY THROUGH BOTH REACTIVE OXYGEN SPECIES DEPENDENT AND INDEPENDENT PATHWAYS

2012· article· en· W2332019989 on OpenAlexaff
Yanpeng Wang, Jian Ma, Wei Meng, Tianqing Peng

Bibliographic record

VenueHeart · 2012
Typearticle
Languageen
FieldMedicine
TopicChemotherapy-induced cardiotoxicity and mitigation
Canadian institutionsWestern University
Fundersnot available
KeywordsDoxorubicinCardiotoxicityReactive oxygen speciesNADPH oxidaseApoptosisRAC1PharmacologyOxidative stressMedicineProgrammed cell deathDNA fragmentationDNA damageCell biologyBiochemistryBiologySignal transductionToxicityEndocrinologyInternal medicineChemotherapy

Abstract

fetched live from OpenAlex

Objectives Doxorubicin causes damage to the heart, often leading to irreversible cardiomyopathy, which is fatal. Reactive oxygen species (ROS) or oxidative stress is involved in cardiomyocyte death, contributing to doxorubicin-induced cardiotoxicity. This study was to investigate the role of Rac1, an important subunit of NADPH oxidase in doxorubicin-induced cardiotoxicity and the underlying mechanisms. Methods The models of doxorubicin-induced cardiotoxicity were created by challenging the mice with 20 mg/kg doxorubicin intraperitoneally. Cardiac function was determined by hemodynamic measurements. Cardiomyocytes apoptosis was assayed by caspase-3 activity assay and DNA fragmentation ELISA. ROS production was measured using DCF-DA molecule probe and NADPH oxidase was measured by an assay kit. We also used a HDAC assay kit to measure HDAC activity of cardiomyocytes. Results In a mouse model of acute doxorubicin-induced cardiotoxicity, cardiomyocyte-specific deletion of Rac1 inhibited NADPH oxidase activation and ROS production, prevented cardiac cell death and improved myocardial function in Rac1 knockout mice. Therapeutic administration of a specific Rac1 inhibitor NSC23766 achieved similar cardioprotective effects of Rac1 inhibition in doxorubicin-stimulated mice. In vitro studies using rat cardiomyoblasts H9c2 cells and neonatal mouse cardiomyocytes demonstrated that Rac1 inhibition attenuated apoptosis as determined by decreases in caspase-3 activity and DNA fragmentation in response to doxorubicin, which correlated with a reduction of ROS production and down-regulation of p53 acetylation and histone H2AX phosphorylation. Doxorubicin also inhibited the activity of classical histone deacetylases (HDAC), which was preserved by Rac1 inhibition. Interestingly, scavenging ROS mitigated apoptosis but did not change HDAC activity and p53 acetylation stimulated by doxorubicin, suggesting both ROS dependent and independent pathways are involved in Rac1-mediated cardiotoxicity. Furthermore, HDAC inhibitor trichostatin A enhanced apoptosis, p53 acetylation and H2AX phosphorylation in doxorubicintreated cardiomyocytes. Conclusions Rac1 signalling contributes to doxorubicin-induced cardiotoxicity through both ROS dependent mechanism and ROS independent HDAC/p53 signalling in cardiomyocytes. Thus, inhibition of Rac1 may be a useful therapy for doxorubicin-induced cardiotoxicity.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.081
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.048
GPT teacher head0.275
Teacher spread0.227 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations4
Published2012
Admission routes1
Has abstractyes

Explore more

Same venueHeartSame topicChemotherapy-induced cardiotoxicity and mitigationFrench-language works237,207