Τίτλος:
Endoplasmic Reticulum Stress and Autophagy in the Pathogenesis of Non-alcoholic Fatty Liver Disease (NAFLD): Current Evidence and Perspectives
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Purpose of Review: Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease with rising prevalence worldwide. Herein, we provide a comprehensive overview of the current knowledge supporting the role of ER stress and autophagy processes in NAFLD pathogenesis and progression. We also highlight the interrelation between these two pathways and the impact of ER stress and autophagy modulators on NAFLD treatment. Recent Findings: The pathophysiological mechanisms involved in NAFLD progression are currently under investigation. The endoplasmic reticulum (ER) stress and the concomitant unfolded protein response (UPR) seem to contribute to its pathogenesis mainly due to high ER content in the liver which exerts significant metabolic functions and can be dysregulated. Furthermore, disruption of autophagy processes has also been identified in NAFLD. The crucial role of these two pathways in NAFLD is underlined by the fact that they have recently emerged as promising targets of therapeutic interventions. Summary: There is a greater need for finding the natural/chemical compounds and drugs which can modulate the ER stress pathway and autophagy for the treatment of NAFLD. Clarifying the inter-relation between these two pathways and their interaction with inflammatory and apoptotic mechanisms will allow the development of additional therapeutic options which can better target and reprogram the underlying pathophysiological pathways, aiming to attenuate NAFLD progression. © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Συγγραφείς:
Flessa, C.-M.
Kyrou, I.
Nasiri-Ansari, N.
Kaltsas, G.
Papavassiliou, A.G.
Kassi, E.
Randeva, H.S.
Περιοδικό:
Current Obesity Reports
Λέξεις-κλειδιά:
acetyl coenzyme A carboxylase; activating transcription factor 4; activating transcription factor 6; activating transcription factor 6 alpha; adipocytokine; angiopoietin like 3; angiopoietin related protein; apolipoprotein B100; autophagy related protein; autophagy related protein 5; autophagy related protein 8 family; basic leucine zipper transcription factor; beclin 1; cantharidin; carboxylesterase; carboxylesterase 1; caveolin 1; CCAAT enhancer binding protein beta; CD40 ligand; corilagin; crocin; cryopyrin; cryptotanshinone; curcumin; diacylglycerol acyltransferase 2; diiodothyronine; dipeptidyl peptidase IV inhibitor; elongation factor 2; empagliflozin; epigallocatechin gallate; exendin 4; ezetimibe; farnesoid X receptor; fat droplet; gallic acid propyl ester; geniposide; glucagon like peptide 1; glucagon like peptide 1 receptor agonist; glucose regulated protein 78; growth arrest and DNA damage inducible protein 153; guanabenz; hypoxia inducible factor 1alpha; immunoglobulin enhancer binding protein; inositol; inositol requiring enzyme 1 alpha; liothyronine; lipoprotein receptor; liraglutide; liver enzyme; mammalian target of rapamycin; mammalian target of rapamycin complex 1; melatonin; metformin; microRNA 214; nuclear receptor DAX 1; nucleotide binding oligomerization domain like receptor; peretinoin; peroxisome proliferator activated receptor gamma; pioglitazone; proprotein convertase 9; protein tyrosine phosphatase; quercetin; resveratrol; rosiglitazone; salubrinal; selonsertib; sequestosome 1; serine threonine protein kinase ULK1; sirtuin 6; sodium glucose cotransporter 2; sterol regulatory element binding protein 2; stress activated protein kinase; tangeretin; taurursodiol; tetrahydrolipstatin; thioredoxin interacting protein; transcription factor FKHR; transcription factor FOXO; transcription factor Nrf2; transforming growth factor beta; unclassified drug; ursodeoxycholic acid; valosin containing protein; X box binding protein 1, adipose tissue; alanine aminotransferase level; apoptosis; aspartate aminotransferase level; autophagy (cellular); body mass; cancer growth; disease exacerbation; endoplasmic reticulum stress; gamma glutamyl transferase blood level; homeostasis; human; hyperglycemia; hyperinsulinemia; inflammation; lipid diet; lipolysis; liver cell carcinoma; non insulin dependent diabetes mellitus; nonalcoholic fatty liver; nonalcoholic steatohepatitis; obesity; oxidative stress; pathogenesis; randomized controlled trial (topic); Review; steatosis; unfolded protein response; animal; autophagy; endoplasmic reticulum stress; liver; metabolism; nonalcoholic fatty liver; pathology; physiology, Animals; Autophagy; Endoplasmic Reticulum Stress; Humans; Liver; Non-alcoholic Fatty Liver Disease; Obesity; Unfolded Protein Response
DOI:
10.1007/s13679-021-00431-3
