Journal
BIOMEDICINES
Volume 11, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines11071961
Keywords
NAFLD; AATD; cardiovascular disease; lipids; meta-inflammation
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Non-alcoholic fatty liver disease (NAFLD) is associated with obesity, dyslipidemia, hypertension, and diabetes, while other diseases like alpha-1 antitrypsin deficiency (AATD) are also linked to liver steatosis. The causes of hepatic lipid deposits can be genetic and epigenetic, with outcomes ranging from benign steatosis to liver failure and extrahepatic diseases. This review explores the similarities and differences between NAFLD and AATD molecular pathways, and highlights the potential of hepatic organoids as novel models for studying liver steatosis.
Non-alcoholic fatty liver disease (NAFLD) is a type of steatosis commonly associated with obesity, dyslipidemia, hypertension, and diabetes. Other diseases such as inherited alpha-1 antitrypsin deficiency (AATD) have also been related to the development of liver steatosis. The primary reasons leading to hepatic lipid deposits can be genetic and epigenetic, and the outcomes range from benign steatosis to liver failure, as well as to extrahepatic diseases. Progressive hepatocellular damage and dysregulated systemic immune responses can affect extrahepatic organs, specifically the heart and lungs. In this review, we discuss the similarities and differences between the molecular pathways of NAFLD and AATD, and the putative value of hepatic organoids as novel models to investigate the physio pathological mechanisms of liver steatosis.
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