ArticleToxicology reports2025
Acute exposure to clozapine and sodium valproate impairs oxidative phosphorylation in human cardiac mitochondria.
Article in Toxicology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The only antipsychotic that is approved and recommended for the treatment of otherwise treatment-resistant schizophrenia is clozapine (CLZ). Unfortunately, CLZ can cause serious cardiotoxicities such as myocarditis and cardiomyopathy. The co-administration of sodium valproate (VPA) during initiation is a well-established risk factor for the development of CLZ-induced myocarditis. However, the mechanisms behind these cardiac adverse effects and the role of VPA co-administration are not understood. Preliminary evidence for the development of cardiac mitochondrial dysfunction has previously been reported in both rodent models and immortalised cell lines. This investigation aimed to determine the functional effects of CLZ and VPA on human cardiac mitochondria to improve the current understanding of how cardiotoxicity develops. Small samples of human atrial tissue from consenting patients undergoing a coronary artery bypass grafting procedure were freshly collected and utilised to investigate the acute effects of each drug on mitochondrial O
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