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PRECLINICAL PUBLICATION · 2019

Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress.

Mouse / Chemical/toxin

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 31580970 ↗2019Reported benefit

Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress.

MouseChemical/toxinC57BL/6Male

Model: Doxorubicin-induced acute cardiotoxicity in mice, with parallel doxorubicin exposure of H9C2 cardiomyoblasts in vitro

Doxorubicin caused acute cardiac injury with reduced cardiac function, increased cardiomyocyte apoptosis and a significant rise in CACNA1H expression. ABT-639 partly protected myocardial function and reduced cardiomyocyte apoptosis, and significantly changed endoplasmic reticulum stress-related pro…

Extraction: extract · Supplied extraction confidence: 0.55. Machine-extracted fields require source verification.