Special Issue "Autophagy in the Liver"
Deadline for manuscript submissions: 30 December 2023 | Viewed by 1488
Interests: clinical microbiology; diagnostics; host-microbial interaction; liver diseases; cancer-infection comorbidities
Interests: host-pathogen interaction; regenerative biology; immunology; microbiology; bacterial drug resistance; metabolic pathways discovery
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Autophagy is a conserved process that catabolizes damaged cellular components to replenish the cells' nutrients for energy and to form new cells. Autophagy plays a critical role in the clearance of pathogens and cellular debris either by direct elimination via lysosomes as part of innate immune responses or by promoting adaptive immunity through antigen processing and presentations. Autophagy was first identified in 1963 by de Duve, who initially observed a form of autophagic vacuoles in the liver. Later on, the autophagy process was defined as the formation of double-membrane autophagosomes in the cytosol, where cytosolic components are enclosed through the elongation of phagophores, followed by the fusion with lysosomes to become degradative autolysosomes. Since then, many studies have been conducted to understand the role of Autophagy in various disease models including liver diseases. Autophagy has been shown to play a role in the development and progression of hepatocellular carcinoma, as well as in the development of metabolic disorders such as obesity, type 2 diabetes, and metabolic dysfunction-associated fatty liver disease (MAFLD). MAFLD is a chronic progressive liver disease that may progress from a benign histological disease stage characterized by non-inflammatory fat accumulation, usually referred to as simple steatosis or nonalcoholic fatty liver (NAFLD), to a more severe form referred to as nonalcoholic steatohepatitis (NASH) characterized by significant liver cell injury, a mixed inflammatory lobular infiltrate, and variable fibrosis that may progress into cirrhosis and liver cancer. The accumulation of lipids and the development of liver damage in these metabolic liver diseases have been linked to an impairment of signaling involved in Autophagy regulation. A complex network of signaling pathways is activated in response to various stimuli, such as nutrient deprivation, stress, and growth factor signaling. These keys signaling pathways/molecules involved in Autophagy include the AMP-activated protein kinase (AMPK), the mammalian target of rapamycin (mTOR) target, and the transcription factor FOXO3. As these pathways also regulate multiple cellular activities where several effectors and regulators are involved, crosstalk between autophagy and other cellular processes exists. The balance between these signaling molecules' activity is essential for the regulation of Autophagy, and disruptions in this balance have been shown to lead to pathological conditions. Thus targeting Autophagy may be a new and important intervention that could improve the outcome of liver diseases in which dysregulated autophagy plays a key role in disease pathogenesis.
This Special Issue accepts submissions of original research articles, reviews, mini-reviews, and commentaries. The focus will be on, but not limited to, the following subtopics:
- Role of autophagy in hepatocellular Carcinoma
- Role of autophagy in metabolic liver diseases such as MAFLD and NASH
- Role of autophagy in chronic viral hepatitis
- The mechanisms of autophagic regulation in acute and chronic liver diseases
- Crosstalk between autophagy and other cellular processes in liver diseases.
- Autophagy-mediated immunomodulation during acute and chronic liver injury
- Development of autophagy-targeted therapy for liver diseases.
Dr. Nahed Ismail
Dr. Aditya Sharma
Manuscript Submission Information
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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- liver diseases
- cellular stress
- viral hepatitis
- liver injury
- hepatocellular carcinoma
- AMPK signaling
- mTOR signaling
- metabolic disorders
- lipid metabolism