Can Na R -alpha Lipoic Acid Damage Liver

Organelles in focus

Mitochondria in not-alcoholic fat liver illness

Under a Creative Commons license

Open access

Highlights

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Increased mitochondrial activeness protects hepatocytes from the deleterious effects of FFAs deposition.

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Hepatic mitochondria are structurally and molecularly contradistinct in NAFLD.

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Mitochondrial dysfunction in animal models of NAFLD is characterized by alterations in the abundance and activity of OXPHOS proteins.

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Decline in mitochondrial function provokes metabolic disturbances and may potentially contribute to NAFLD progression.

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Increased mitochondrial cholesterol accumulation is related with the progression of steatosis to steatohepatitis.

Abstract

NAFLD is a mutual disease in Western society and ranges from steatosis to steatohepatitis and to end-phase liver disease. The molecular mechanisms that crusade the progression of steatosis to severe liver damage are non fully understood. 1 suggested mechanism involves the oxidation of biomolecules past mitochondrial ROS which initiates a cruel bike of exacerbated mitochondrial dysfunction and increased hepatocellular oxidative damage. This may ultimately pave the way for hepatic inflammation and liver failure. This review updates our current agreement of mitochondria-derived oxidative stress in the progression of NAFLD.

Abbreviations

8-OHdG

8-hydroxy-2-deoxyguanosine

Δy_m

mitochondrial membrane potential

AMPK

AMP-activated protein kinase

AST

aspartate transaminase

ATP

adenosine triphosphate

CPT-1

carnitine palmitoyl-transferase 1

ETC

electron transport chain

Gpx

glutathione peroxidase

iNOS

inducible nitric oxide synthase

JNK

c-JunNH_ii-final kinase

MPT

mitochondrial permeability transition

NADPH

nicotinamide adenine dinucleotide phosphate

NAFLD

non-alcoholic fatty liver disease

NASH

non-alcoholic steatohepatitis

NF-κB

nuclear gene kappa-B

NRF-2

nuclear respiratory factor 2

OXPHOS

oxidative phosphorylation

PGC-1α

peroxisome proliferative activated receptor-gamma coactivator-1α

PPAR-α

peroxisome proliferator activated receptor-α

RNS

reactive nitrogen species

ROS

Reactive oxygen species

SOD2

superoxide dismutase two

TFAM

mitochondrial transcription gene A

TNF-α

tumor necrosis factor- α

UPR

unfolded protein response

VLDL

very low density lipoprotein

Keywords

Mitochondria

Steatosis

ROS

NAFLD

NASH

© 2022 The Authors. Published by Elsevier Ltd.

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Source: https://www.sciencedirect.com/science/article/pii/S1357272517303321