Extracellular Vesicles as Inflammatory Drivers in NAFLD

Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease in most parts of the world affecting one-third of the western population and a growing cause for end-stage liver diseases such as hepatocellular carcinoma (HCC). Majorly driven by obesity and diabetes mellitus, NAF...

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Main Authors: Akshatha N. Srinivas, Diwakar Suresh, Prasanna K. Santhekadur, Deepak Suvarna, Divya P. Kumar
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-02-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2020.627424/full
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author Akshatha N. Srinivas
Diwakar Suresh
Prasanna K. Santhekadur
Deepak Suvarna
Divya P. Kumar
author_facet Akshatha N. Srinivas
Diwakar Suresh
Prasanna K. Santhekadur
Deepak Suvarna
Divya P. Kumar
author_sort Akshatha N. Srinivas
collection DOAJ
description Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease in most parts of the world affecting one-third of the western population and a growing cause for end-stage liver diseases such as hepatocellular carcinoma (HCC). Majorly driven by obesity and diabetes mellitus, NAFLD is more of a multifactorial disease affected by extra-hepatic organ crosstalk. Non-alcoholic fatty liver (NAFL) progressed to non-alcoholic steatohepatitis (NASH) predisposes multiple complications such as fibrosis, cirrhosis, and HCC. Although the complete pathogenic mechanisms of this disease are not understood, inflammation is considered as a key driver to the onset of NASH. Lipotoxicity, inflammatory cytokines, chemokines, and intestinal dysbiosis trigger both hepatic and systemic inflammatory cascades simultaneously activating immune responses. Over a few years, extracellular vesicles studied extensively concerning the pathobiology of NAFLD indicated it as a key modulator in the setting of immune-mediated inflammation. Exosomes and microvesicles, the two main types of extracellular vesicles are secreted by an array of most mammalian cells, which are involved mainly in cell-cell communication that are unique to cell type. Various bioactive cargoes containing extracellular vesicles derived from both hepatic and extrahepatic milieu showed critical implications in driving steatosis to NASH reaffirming inflammation as the primary contributor to the whole process. In this mini-review, we provide brief insights into the inflammatory mediators of NASH with special emphasis on extracellular vesicles that acts as drivers of inflammation in NAFLD.
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spelling doaj.art-7b1c6eeab7c4490189a66dfb9b0d29ad2022-12-21T21:28:31ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-02-011110.3389/fimmu.2020.627424627424Extracellular Vesicles as Inflammatory Drivers in NAFLDAkshatha N. Srinivas0Diwakar Suresh1Prasanna K. Santhekadur2Deepak Suvarna3Divya P. Kumar4Department of Biochemistry, CEMR, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, IndiaDepartment of Biochemistry, CEMR, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, IndiaDepartment of Biochemistry, CEMR, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, IndiaDepartment of Gastroenterology, JSS Medical College and Hospital, JSS Academy of Higher Education and Research, Mysuru, IndiaDepartment of Biochemistry, CEMR, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, IndiaNon-alcoholic fatty liver disease (NAFLD) is a highly prevalent chronic liver disease in most parts of the world affecting one-third of the western population and a growing cause for end-stage liver diseases such as hepatocellular carcinoma (HCC). Majorly driven by obesity and diabetes mellitus, NAFLD is more of a multifactorial disease affected by extra-hepatic organ crosstalk. Non-alcoholic fatty liver (NAFL) progressed to non-alcoholic steatohepatitis (NASH) predisposes multiple complications such as fibrosis, cirrhosis, and HCC. Although the complete pathogenic mechanisms of this disease are not understood, inflammation is considered as a key driver to the onset of NASH. Lipotoxicity, inflammatory cytokines, chemokines, and intestinal dysbiosis trigger both hepatic and systemic inflammatory cascades simultaneously activating immune responses. Over a few years, extracellular vesicles studied extensively concerning the pathobiology of NAFLD indicated it as a key modulator in the setting of immune-mediated inflammation. Exosomes and microvesicles, the two main types of extracellular vesicles are secreted by an array of most mammalian cells, which are involved mainly in cell-cell communication that are unique to cell type. Various bioactive cargoes containing extracellular vesicles derived from both hepatic and extrahepatic milieu showed critical implications in driving steatosis to NASH reaffirming inflammation as the primary contributor to the whole process. In this mini-review, we provide brief insights into the inflammatory mediators of NASH with special emphasis on extracellular vesicles that acts as drivers of inflammation in NAFLD.https://www.frontiersin.org/articles/10.3389/fimmu.2020.627424/fullexosomesmicrovesiclesnonalcoholic fatty liver diseaseinflammationcytokinesimmune system
spellingShingle Akshatha N. Srinivas
Diwakar Suresh
Prasanna K. Santhekadur
Deepak Suvarna
Divya P. Kumar
Extracellular Vesicles as Inflammatory Drivers in NAFLD
Frontiers in Immunology
exosomes
microvesicles
nonalcoholic fatty liver disease
inflammation
cytokines
immune system
title Extracellular Vesicles as Inflammatory Drivers in NAFLD
title_full Extracellular Vesicles as Inflammatory Drivers in NAFLD
title_fullStr Extracellular Vesicles as Inflammatory Drivers in NAFLD
title_full_unstemmed Extracellular Vesicles as Inflammatory Drivers in NAFLD
title_short Extracellular Vesicles as Inflammatory Drivers in NAFLD
title_sort extracellular vesicles as inflammatory drivers in nafld
topic exosomes
microvesicles
nonalcoholic fatty liver disease
inflammation
cytokines
immune system
url https://www.frontiersin.org/articles/10.3389/fimmu.2020.627424/full
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AT prasannaksanthekadur extracellularvesiclesasinflammatorydriversinnafld
AT deepaksuvarna extracellularvesiclesasinflammatorydriversinnafld
AT divyapkumar extracellularvesiclesasinflammatorydriversinnafld