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Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods
by
Mihajlovic, Milos
, Vinken, Mathieu
in
Amino acids
/ Ammonia
/ Apoptosis
/ Carbon
/ Chemical and Drug Induced Liver Injury - diagnosis
/ Chemical and Drug Induced Liver Injury - etiology
/ Chemical and Drug Induced Liver Injury - metabolism
/ Cytoplasm
/ Dehydrogenases
/ Dihydrofolate reductase
/ DNA methylation
/ Drug development
/ Drug-Related Side Effects and Adverse Reactions - metabolism
/ Energy
/ Enzymes
/ Fatty acids
/ Glucose
/ Glycerol
/ Homeostasis
/ Humans
/ Liver
/ Liver - metabolism
/ Metabolism
/ Metabolites
/ Mitochondria
/ Mitochondria - metabolism
/ Mitochondria, Liver - metabolism
/ Mitochondrial DNA
/ Oxidation
/ Patient safety
/ Polyamines
/ Proteins
/ Review
2022
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Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods
by
Mihajlovic, Milos
, Vinken, Mathieu
in
Amino acids
/ Ammonia
/ Apoptosis
/ Carbon
/ Chemical and Drug Induced Liver Injury - diagnosis
/ Chemical and Drug Induced Liver Injury - etiology
/ Chemical and Drug Induced Liver Injury - metabolism
/ Cytoplasm
/ Dehydrogenases
/ Dihydrofolate reductase
/ DNA methylation
/ Drug development
/ Drug-Related Side Effects and Adverse Reactions - metabolism
/ Energy
/ Enzymes
/ Fatty acids
/ Glucose
/ Glycerol
/ Homeostasis
/ Humans
/ Liver
/ Liver - metabolism
/ Metabolism
/ Metabolites
/ Mitochondria
/ Mitochondria - metabolism
/ Mitochondria, Liver - metabolism
/ Mitochondrial DNA
/ Oxidation
/ Patient safety
/ Polyamines
/ Proteins
/ Review
2022
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Do you wish to request the book?
Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods
by
Mihajlovic, Milos
, Vinken, Mathieu
in
Amino acids
/ Ammonia
/ Apoptosis
/ Carbon
/ Chemical and Drug Induced Liver Injury - diagnosis
/ Chemical and Drug Induced Liver Injury - etiology
/ Chemical and Drug Induced Liver Injury - metabolism
/ Cytoplasm
/ Dehydrogenases
/ Dihydrofolate reductase
/ DNA methylation
/ Drug development
/ Drug-Related Side Effects and Adverse Reactions - metabolism
/ Energy
/ Enzymes
/ Fatty acids
/ Glucose
/ Glycerol
/ Homeostasis
/ Humans
/ Liver
/ Liver - metabolism
/ Metabolism
/ Metabolites
/ Mitochondria
/ Mitochondria - metabolism
/ Mitochondria, Liver - metabolism
/ Mitochondrial DNA
/ Oxidation
/ Patient safety
/ Polyamines
/ Proteins
/ Review
2022
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Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods
Journal Article
Mitochondria as the Target of Hepatotoxicity and Drug-Induced Liver Injury: Molecular Mechanisms and Detection Methods
2022
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Overview
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.
Publisher
MDPI AG,MDPI
Subject
/ Ammonia
/ Carbon
/ Chemical and Drug Induced Liver Injury - diagnosis
/ Chemical and Drug Induced Liver Injury - etiology
/ Chemical and Drug Induced Liver Injury - metabolism
/ Drug-Related Side Effects and Adverse Reactions - metabolism
/ Energy
/ Enzymes
/ Glucose
/ Glycerol
/ Humans
/ Liver
/ Mitochondria, Liver - metabolism
/ Proteins
/ Review
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