期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/ijms23063315
关键词
hepatotoxicity; liver injury; mitochondrial dysfunction; molecular mechanisms; in vitro
资金
- Marie Sklodowska-Curie COFUND Action [101034352]
- European Horizon 2020 framework program [858014, 963845]
- US Alternatives Research and Development Foundation [2021]
- Research Foundation Flanders [G070422N]
- Methusalem program of the Flemish government [2021]
- Scientific Fund Willy Gepts [2021]
- Marie Curie Actions (MSCA) [101034352] Funding Source: Marie Curie Actions (MSCA)
Drug-induced liver injury is often associated with mitochondrial perturbation and dysfunction. While many methods have been developed to study mitochondrial function, there is a need for more liver physiology-based models and approaches to predict potential toxicity and reduce clinical complications.
One of the major mechanisms of drug-induced liver injury includes mitochondrial perturbation and dysfunction. This is not a surprise, given that mitochondria are essential organelles in most cells, which are responsible for energy homeostasis and the regulation of cellular metabolism. Drug-induced mitochondrial dysfunction can be influenced by various factors and conditions, such as genetic predisposition, the presence of metabolic disorders and obesity, viral infections, as well as drugs. Despite the fact that many methods have been developed for studying mitochondrial function, there is still a need for advanced and integrative models and approaches more closely resembling liver physiology, which would take into account predisposing factors. This could reduce the costs of drug development by the early prediction of potential mitochondrial toxicity during pre-clinical tests and, especially, prevent serious complications observed in clinical settings.
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