Cellular and Molecular Mechanisms Underlying the Pathogenesis of Fat Accumulation and Disease Progression in NAFLD
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Intracellular and Plasma Membranes".
Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 1853
Special Issue Editors
Interests: liver diseases; liver cirrhosis; biliary tract diseases; liver transplantation; cholangiocarcinoma
2. Department of Science and Technology for Humans and the Environment, Università Campus Bio-Medico di Roma, Via Álvaro del Portillo 21, 00128 Rome, Italy
Interests: gastro-esophageal reflux disease; pathophysiology; diagnosis; and treatment; gas-trointestinal motility; functional disorders of the gastrointestinal tract; diagnosis and treatment of inflammatory bowel disease
Special Issues, Collections and Topics in MDPI journals
Interests: liver disease; non-alcoholic fatty liver disease; non-alcoholic statohepatitis; liver tumors; cell biology
Interests: liver disease; intestinal microbiota; non-alcoholic fatty liver diseases
Special Issue Information
Dear Colleagues,
Among the different metabolic tasks, a leading role in liver metabolism is covered by mechanisms involved in fat storage and disposal. A derangement at any point of this complex machinery could lead to NAFLD, the most common liver disease worldwide widespread. In recent years, increasing evidence has accumulated on the different molecular mechanisms involved in NAFLD pathogenesis and in the progression from simple steatosis to steato-hepatitis and fibrosis and, eventually, cancer. A number of genetic risk factors for NAFLD/NASH susceptibility and progression have been individuated and other are currently under investigation (e.g. PNPLA3, TM6SF2, etc…). Furthermore, hepatic gene expression profile analysis has been found useful in distinguishing individuals with a different outcome in the spectrum of NAFLD severity. In recent years, a novel field called epigenetics reveals changes in gene expression unrelated to modifications to the underlying DNA sequence and linked to NAFLD. DNA methylation and non-coding RNA are found to be a major determinant of disease progression and further studies are needed to corroborate their pathogenetic and prognostic role. The liver fat accumulation is also caused by distant organ dysfunction. Recently the gut-liver axis was found to play an important role in liver inflammation and NAFLD progression. Gut microbiome composition, bacterial products (metabolome), and an alteration of gut mucosal barrier (the so-called “leaky gut”) were linked to inflammation and fibrosis in NAFLD. Finally, evidence regarding the deregulation of pathways that control de novo lipogenesis and fat catabolism, including the lipophagy pathway, is gaining increasing attention, as well as the clinical relevance of a reduction in the activity of several lipases, key enzymes for the disposal of intracellular fat. In this Special Issue of Cells, I invite you to contribute original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “Cellular and Molecular Mechanisms underlying the Pathogenesis of fat accumulation and disease progression in NAFLD”. Expert articles describing mechanistic, functional, cellular, biochemical, or general aspects of NAFLD are highly welcome. Relevant topics include but are not limited to:
-NASH/NAFLD
-genetics-epigenetics
-gut-liver axis
-microbiome-metabolome
-lipid metabolism-inflammation
-lipophagy
-In vitro and in vivo models
Dr. Simone Carotti
Dr. Annamaria Altomare
Dr. Maria Francesconi
Dr. Francesco Valentini
Dr. Umberto Vespasiani-Gentilucci
Guest Editors
Manuscript Submission Information
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Keywords
- Non-alcoholic fatty liver disease/Non-alcoholic statohepatitis
- genetics
- epigenetics
- gut-liver axis
- microbiome
- metabolome
- lipid metabolism
- inflammation
- lipophagy
- In vitro and in vivo models
