Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Molecular Mechanisms of Drug-Induced, Immune-Mediated Liver Injury
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Molecular Mechanisms of Drug-Induced, Immune-Mediated Liver Injury

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 9876

Special Issue Editors

Dr. Dolores B. Njoku

E-Mail Website
Guest Editor
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, MD 21287, USA
Interests: immunology; B cells; Tregs; liver injury; drug-induced; immune-mediated
Special Issues, Collections and Topics in MDPI journals
Dr. Munish Puri

E-Mail Website
Guest Editor
UMass Chan Medical School, Worcester, MA 01605, USA
Interests: liver injury; DILI liver toxicity; NASH; immunology; oncology; computational pathology; spatial transcriptomics; computational genomics; artificial intelligence
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Liver disease and cirrhosis are the sixth most common cause of death in adults between the ages of 25 and 64. Drug-induced hepatitis is a type of liver disease and a leading cause of acute liver failure. Drug-induced, immune-mediated liver injury is the most common hepatic, immune-mediated liver disease and is a common reason an approved medication being removed from the consumer market. Current evidence suggests that susceptible individuals can develop drug-induced, immune-mediated liver injury after receiving halogenated anesthetics, antiseizure medications, antibiotics, antivirals, antihypertensives, or nonsteroidal anti-inflammatory drugs. A major challenge to understanding the pathogenesis of drug-induced, immune-mediated liver injury is its diverse presentations, which can range from toxic hepatitis-induced acute liver failure to immune-mediated hepatitis with autoimmune features. Precise understanding of the molecular mechanisms of drug-induced, immune-mediated liver injury through basic, translational, and clinical studies is critical in order to reduce significant morbidity in patients, unanticipated costs to patients and hospitals, and to completely address this disease. The key molecular mechanisms that initiate drug-induced, immune-mediated liver injury have been uncovered, and the mechanisms that modulate disease severity are now being discovered.  Our goal in this Special Issue is to convey the mechanisms that regulate the severity of DIH using in vitro models, animal models, in silico studies, and human studies that might uncover therapeutic targets or mechanisms that regulate morbidity or mortality of drug-induced, immune-mediated liver injury in patients.

Dr. Dolores B. Njoku
Dr. Munish Puri
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

21 pages, 631 KiB  
Review
Immune-Mediated Drug-Induced Liver Injury: Immunogenetics and Experimental Models
by Alessio Gerussi, Ambra Natalini, Fabrizio Antonangeli, Clara Mancuso, Elisa Agostinetto, Donatella Barisani, Francesca Di Rosa, Raul Andrade and Pietro Invernizzi
Int. J. Mol. Sci. 2021, 22(9), 4557; https://doi.org/10.3390/ijms22094557 - 27 Apr 2021
Cited by 40 | Viewed by 5525
Abstract
Drug-induced liver injury (DILI) is a challenging clinical event in medicine, particularly because of its ability to present with a variety of phenotypes including that of autoimmune hepatitis or other immune mediated liver injuries. Limited diagnostic and therapeutic tools are available, mostly because [...] Read more.
Drug-induced liver injury (DILI) is a challenging clinical event in medicine, particularly because of its ability to present with a variety of phenotypes including that of autoimmune hepatitis or other immune mediated liver injuries. Limited diagnostic and therapeutic tools are available, mostly because its pathogenesis has remained poorly understood for decades. The recent scientific and technological advancements in genomics and immunology are paving the way for a better understanding of the molecular aspects of DILI. This review provides an updated overview of the genetic predisposition and immunological mechanisms behind the pathogenesis of DILI and presents the state-of-the-art experimental models to study DILI at the pre-clinical level. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Drug-Induced, Immune-Mediated Liver Injury)
►▼ Show Figures

Figure 1

19 pages, 3544 KiB  
Review
The Role of Hypoxia-Induced Mitogenic Factor in Organ-Specific Inflammation in the Lung and Liver: Key Concepts and Gaps in Knowledge Regarding Molecular Mechanisms of Acute or Immune-Mediated Liver Injury
by Sananda Pai and Dolores B. Njoku
Int. J. Mol. Sci. 2021, 22(5), 2717; https://doi.org/10.3390/ijms22052717 - 8 Mar 2021
Cited by 3 | Viewed by 3678
Abstract
Hypoxia-induced mitogenic factor (HIMF), which is also known as resistin-like molecule α (RELM-α), found in inflammatory zone 1 (FIZZ1), or resistin-like alpha (retlna), is a cysteine-rich secretory protein and cytokine. HIMF has been investigated in the lung as a mediator of pulmonary fibrosis, [...] Read more.
Hypoxia-induced mitogenic factor (HIMF), which is also known as resistin-like molecule α (RELM-α), found in inflammatory zone 1 (FIZZ1), or resistin-like alpha (retlna), is a cysteine-rich secretory protein and cytokine. HIMF has been investigated in the lung as a mediator of pulmonary fibrosis, inflammation and as a marker for alternatively activated macrophages. Although these macrophages have been found to have a role in acute liver injury and acetaminophen toxicity, few studies have investigated the role of HIMF in acute or immune-mediated liver injury. The aim of this focused review is to analyze the literature and examine the effects of HIMF and its human homolog in organ-specific inflammation in the lung and liver. We followed the guidelines set by PRISMA in constructing this review. The relevant checklist items from PRISMA were included. Items related to meta-analysis were excluded because there were no randomized controlled clinical trials. We found that HIMF was increased in most models of acute liver injury and reduced damage from acetaminophen-induced liver injury. We also found strong evidence for HIMF as a marker for alternatively activated macrophages. Our overall risk of bias assessment of all studies included revealed that 80% of manuscripts demonstrated some concerns in the randomization process. We also demonstrated some concerns (54.1%) and high risk (45.9%) of bias in the selection of the reported results. The need for randomization and reduction of bias in the reported results was similarly detected in the studies that focused on HIMF and the liver. In conclusion, we propose that HIMF could be utilized as a marker for M2 macrophages in immune-mediated liver injury. However, we also detected the need for randomized clinical trials and additional experimental and human prospective studies in order to fully comprehend the role of HIMF in acute or immune-mediated liver injury. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Drug-Induced, Immune-Mediated Liver Injury)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop