Special Issue "Autophagy in the Liver"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: 30 December 2023 | Viewed by 1488

Special Issue Editors

Medical Director, Clinical Microbiology, Laboratory Medicine, University of Illinois at Chicago (UIC)—College of Medicine University of Illinois Hospitals & Health Science System (UI Health), 840 South Wood Street, 260F CMET (MC 847), Chicago, IL 60612, USA
Interests: clinical microbiology; diagnostics; host-microbial interaction; liver diseases; cancer-infection comorbidities
Department of Pathology, College of Medicine, University of Illinois, Chicago, IL 60612, USA
Interests: host-pathogen interaction; regenerative biology; immunology; microbiology; bacterial drug resistance; metabolic pathways discovery
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Special Issue Information

Dear Colleagues,

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:

  1. Role of autophagy in hepatocellular Carcinoma
  2. Role of autophagy in metabolic liver diseases such as MAFLD and NASH
  3. Role of autophagy in chronic viral hepatitis
  4. The mechanisms of autophagic regulation in acute and chronic liver diseases
  5. Crosstalk between autophagy and other cellular processes in liver diseases.
  6. Autophagy-mediated immunomodulation during acute and chronic liver injury
  7. Development of autophagy-targeted therapy for liver diseases.

Dr. Nahed Ismail
Dr. Aditya Sharma
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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.


  • autophagy
  • liver diseases
  • inflammation
  • cellular stress
  • viral hepatitis
  • NASH
  • liver injury
  • steatosis
  • cirrhosis
  • hepatocellular carcinoma
  • AMPK signaling
  • mTOR signaling
  • metabolic disorders
  • lipid metabolism

Published Papers (2 papers)

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4 pages, 209 KiB  
Role of Autophagy in Ehrlichia-Induced Liver Injury
Cells 2023, 12(9), 1334; https://doi.org/10.3390/cells12091334 - 07 May 2023
Cited by 1 | Viewed by 790
Autophagy is a cellular process that involves the cell breakdown and recycling of cellular components, such as old, damaged, or abnormal proteins, for important cellular functions including development, immune function, stress, and starvation [...] Full article
(This article belongs to the Special Issue Autophagy in the Liver)


Jump to: Editorial

15 pages, 853 KiB  
Non-Canonical Inflammasome Pathway: The Role of Cell Death and Inflammation in Ehrlichiosis
Cells 2023, 12(22), 2597; https://doi.org/10.3390/cells12222597 - 09 Nov 2023
Viewed by 390
Activating inflammatory caspases and releasing pro-inflammatory mediators are two essential functions of inflammasomes which are triggered in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs). The canonical inflammasome pathway involves the activation of inflammasome and its downstream pathway via the [...] Read more.
Activating inflammatory caspases and releasing pro-inflammatory mediators are two essential functions of inflammasomes which are triggered in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs). The canonical inflammasome pathway involves the activation of inflammasome and its downstream pathway via the adaptor ASC protein, which causes caspase 1 activation and, eventually, the cleavage of pro-IL-1b and pro-IL-18. The non-canonical inflammasome pathway is induced upon detecting cytosolic lipopolysaccharide (LPS) by NLRP3 inflammasome in Gram-negative bacteria. The activation of NLRP3 triggers the cleavage of murine caspase 11 (human caspase 4 or caspase 5), which results in the formation of pores (via gasdermin) to cause pyroptosis. Ehrlichia is an obligately intracellular bacterium which is responsible for causing human monocytic ehrlichiosis (HME), a potentially lethal disease similar to toxic shock syndrome and septic shock syndrome. Several studies have indicated that canonical and non-canonical inflammasome activation is a crucial pathogenic mechanism that induces dysregulated inflammation and host cellular death in the pathophysiology of HME. Mechanistically, the activation of canonical and non-canonical inflammasome pathways affected by virulent Ehrlichia infection is due to a block in autophagy. This review aims to explore the significance of non-canonical inflammasomes in ehrlichiosis, and how the pathways involving caspases (with the exception of caspase 1) contribute to the pathophysiology of severe and fatal ehrlichiosis. Improving our understanding of the non-canonical inflammatory pathway that cause cell death and inflammation in ehrlichiosis will help the advancement of innovative therapeutic, preventative, and diagnostic approaches to the treatment of ehrlichiosis. Full article
(This article belongs to the Special Issue Autophagy in the Liver)
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