Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)

Pallavi Subramanian; Jochen Hampe; Frank Tacke; Triantafyllos Chavakis

doi:10.3390/ijms23136996

Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)

Pallavi Subramanian
, Jochen Hampe
, Frank Tacke
, Triantafyllos Chavakis

Research output: Contribution to journal › Review article › peer-review

23 Scopus citations

Abstract

The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re‐defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non‐alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH‐related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte–HSC and macrophage–HSC crosstalk.

Original language	English
Article number	6996
Journal	International Journal of Molecular Sciences
Volume	23
Issue number	13
DOIs	https://doi.org/10.3390/ijms23136996
State	Published - 1 Jul 2022
Externally published	Yes

Keywords

fibrosis
hepatic stellate cells
hepatocyte
macrophage
metabolic associated fatty liver disease
nonalcoholic fatty liver disease
nonalcoholic steatohepatitis

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10.3390/ijms23136996

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title = "Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)",

abstract = "The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re‐defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting \textasciitilde{}25\% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non‐alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH‐related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte–HSC and macrophage–HSC crosstalk.",

keywords = "fibrosis, hepatic stellate cells, hepatocyte, macrophage, metabolic associated fatty liver disease, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis",

author = "Pallavi Subramanian and Jochen Hampe and Frank Tacke and Triantafyllos Chavakis",

note = "Publisher Copyright: {\textcopyright} 2022 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2022",

month = jul,

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doi = "10.3390/ijms23136996",

language = "English",

volume = "23",

journal = "International Journal of Molecular Sciences",

issn = "1661-6596",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

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TY - JOUR

T1 - Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)

AU - Subramanian, Pallavi

AU - Hampe, Jochen

AU - Tacke, Frank

AU - Chavakis, Triantafyllos

PY - 2022/7/1

Y1 - 2022/7/1

N2 - The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re‐defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non‐alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH‐related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte–HSC and macrophage–HSC crosstalk.

AB - The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re‐defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non‐alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH‐related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte–HSC and macrophage–HSC crosstalk.

KW - fibrosis

KW - hepatic stellate cells

KW - hepatocyte

KW - macrophage

KW - metabolic associated fatty liver disease

KW - nonalcoholic fatty liver disease

KW - nonalcoholic steatohepatitis

UR - https://www.scopus.com/pages/publications/85132391162

U2 - 10.3390/ijms23136996

DO - 10.3390/ijms23136996

M3 - Review article

AN - SCOPUS:85132391162

SN - 1661-6596

VL - 23

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

IS - 13

M1 - 6996

ER -

Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)

Abstract

Keywords

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