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Inhibition of mitochondrial beta-oxidation as a mechanism of hepatotoxicity.
TLDR
Drugs and some endogenous compounds can sequester coenzyme A and/or inhibit mitochondrial beta-oxidation enzymes, and decrease mitochondrial DNA replication (dideoxynucleoside analogues), while other compounds act through a combination of different mechanisms.
Mitochondrial dysfunction in NASH: causes, consequences and possible means to prevent it.
TLDR
There is accumulating evidence that mitochondrial dysfunction (more particularly respiratory chain deficiency) plays a key role in the physiopathology of NASH whatever its initial cause and that several drugs can prevent or even reverse NASH.
Drug-induced toxicity on mitochondria and lipid metabolism: mechanistic diversity and deleterious consequences for the liver.
TLDR
In obese and diabetic patients, some drugs may induce acute liver injury more frequently while others may worsen the pre-existent steatosis (or steatohepatitis), which is characterized not only by lipid accumulation but also by necroinflammation and fibrosis.
NASH: a mitochondrial disease.
TLDR
The purpose of this review is to discuss the evidence, mechanisms and implications of mitochondrial dysfunction at the successive steps leading to NASH, as already partially reviewed elsewhere.
Mitochondrial adaptations and dysfunctions in nonalcoholic fatty liver disease
TLDR
Developing drugs that further increase mtFAO and restore MRC activity in a coordinated manner could ameliorate steatosis, but also necroinflammation and fibrosis by reducing oxidative stress.
Mitochondria in steatohepatitis.
TLDR
In patients with steatosis, mitochondrial ROS may oxidize hepatic fat deposits, as suggested in animal models, and lipid peroxidation products impair the flow of electrons along the respiratory chain, which may cause overreduction of respiratory chain components, further increasing mitochondrial ROS formation and lipidPeroxidation.
Drug‐induced liver injury through mitochondrial dysfunction: mechanisms and detection during preclinical safety studies
TLDR
In vitro and in vivo investigations can be performed to determine if newly developed drugs disturb mitochondrial fatty acid oxidation and the oxidative phosphorylation process, deplete hepatic mitochondrial DNA, or trigger the opening of the mitochondrial permeability transition (MPT) pore, as drugs can be deleterious for hepatic mitochondria in some individuals but not in others.
Nonalcoholic steatosis and steatohepatitis. V. Mitochondrial dysfunction in steatohepatitis.
TLDR
Rich diet and lack of exercise are causing a surge in the prevalence of obesity and hepatic steatosis, which causes "primary" steatohepatitis in some patients, which could cause more lipid peroxidation, cytokine induction, and fibrogenesis than in primary steato hepatitis.
The ins and outs of mitochondrial dysfunction in NASH.
TLDR
Reducing the incidence of NASH will be a major challenge for hepatologists for the next decade because some genetic polymorphisms can significantly increase the risk of steatohepatitis and that several drugs can prevent or even reverse NASH.
Increased expression of cytochrome P450 2E1 in nonalcoholic fatty liver disease: mechanisms and pathophysiological role.
TLDR
Higher hepatic CYP2E1 activity during NAFLD could play a significant role in the pathophysiology of NASH by inducing lipid peroxidation and oxidative damage of key cellular components, and CYP1-mediated overproduction of ROS could promote hepatic insulin resistance, which can further aggravate fatty liver.
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