Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

G-protein Inactivator RGS6 Mediates Myocardial Cell Apoptosis and Cardiomyopathy Caused By Doxorubicin

21 Jan 2013

Abstract excerpt

Clinical use of the widely used chemotherapeutic agent doxorubicin is limited by life-threatening cardiotoxicity. The mechanisms underlying doxorubicin-induced cardiomyopathy and heart failure remain unclear but are thought to involve p53-mediated myocardial cell apoptosis. The tripartite G-protein inactivating protein RGS6 has been implicated in reactive oxygen species (ROS) generation, ATM/p53 activation, and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chemotherapy-induced cardiotoxicity and mitigation
Share to Neuroblastoma Research and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23338613
DOI: 10.1158/0008-5472.can-12-3453

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

G-protein Inactivator RGS6 Mediates Myocardial Cell Apoptosis and Cardiomyopathy Caused By DoxorubicinPMID 23338613Read ↗

Regulator of G protein signaling 6 is a critical mediator of both reward-related behavioral and pathological responses to alcoholSemantic proximity Read ↗

Thousand and one amino acid protein kinase 1 suppression improves doxorubicin-induced cardiomyopathy by preventing cardiomyocyte death and dysfunctionSemantic proximity Read ↗

Transcriptomic profiling reveals p53 as a key regulator of doxorubicin-induced cardiotoxicitySemantic proximity Read ↗

Sex Differences in Doxorubicin‐Induced Cardiotoxicity: Insights from Transcriptome AnalysisSemantic proximity Read ↗

m6A demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3Semantic proximity Read ↗

Diminished molecular response to doxorubicin and loss of cardioprotective effect of dexrazoxane in Egr-1 deficient female mice.Semantic proximity Read ↗

Decreased Soluble Guanylate Cyclase Contributes to Cardiac Dysfunction Induced by Chronic Doxorubicin Treatment in Mice.Semantic proximity Read ↗

Substrain-Dependent Differences in Doxorubicin-Induced Cardiotoxicity in Adult C57BL/6 Mice.Semantic proximity Read ↗

Inhibit of the cGAS-STING-STAT1 pathway protects heart from the Doxorubicin-induced cardiotoxicitySemantic proximity Read ↗

Age-Dependent RGS5 Loss in Pericytes Induces Cardiac Dysfunction and FibrosisSemantic proximity Read ↗

Absence of Rgs5 prolongs cardiac repolarization and predisposes to ventricular tachyarrhythmia in mice.Semantic proximity Read ↗

ATF4 alleviates doxorubicin-induced cardiomyopathy through H <sub>2</sub> S-mediated antioxidationSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.