Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Molecular Insight into Human Diseases: Application of Animal Models
share announcement

Molecular Insight into Human Diseases: Application of Animal Models

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 2843

Special Issue Editors

Prof. Dr. Sabry Mohamed Attia

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
Interests: animal model; diabetes; obesity; neurodevelopmental disorder; multiple sclerosis; autism spectrum disorder; rheumatoid arthritis; inflammation; preclinical studies; drug therapy
Dr. Adrian-Bogdan Țigu

E-Mail Website
Guest Editor
MedFuture Research Center for Advanced Medicine, “Iuliu Hațieganu” University of Medicine and Pharmacy, 400377 Cluj-Napoca, Romania
Interests: signaling pathways; biochemistry; cell-culture; cell death mechanism; cancer research; hematology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The study of human diseases and the development of effective therapeutics for these disorders are dependent on the availability of disease-specific model systems. Murine models are considered excellent preclinical research tools in the field of medical research because they provide insights into the complex ecology of human diseases. Murine models have been employed successfully in the study of pathophysiological systems involved in a variety of human diseases because they are repeatable and can sufficiently mimic human disease events.

Authors are invited to submit original articles and reviews that contribute to an enhanced understanding of the following topics: the application of animal models in understanding the pathophysiology of several human diseases, and the utilization of animal models in therapeutic approaches to diabetes, obesity, autism, rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and many others. Authors are also welcome to contribute developing research addressing the utilization of cellular models, with a particular emphasis on the study of in vitro cultured cellular systems, including cell interactions that mimic human disease events.

Prof. Dr. Sabry Mohamed Attia
Dr. Adrian-Bogdan Țigu
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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.

Keywords

  • animal model
  • diabetes
  • obesity
  • neurodevelopmental disorder
  • multiple sclerosis
  • autism spectrum disorder
  • rheumatoid arthritis
  • inflammation
  • preclinical studies
  • drug therapy

Published Papers (3 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:

Research

Jump to: Review

14 pages, 1805 KiB  
Article
Carfilzomib Mitigates Lipopolysaccharide/D-Galactosamine/Dimethylsulfoxide-Induced Acute Liver Failure in Mice
by Dhafer Y. Alhareth, Abdulrazaq Alanazi, Wael A. Alanazi, Mushtaq A. Ansari, Mahmoud N. Nagi, Sheikh F. Ahmad, Mohamed S. M. Attia, Ahmed Nadeem, Saleh A. Bakheet and Sabry M. Attia
Biomedicines 2023, 11(11), 3098; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11113098 - 20 Nov 2023
Viewed by 878
Abstract
Acute liver failure (ALF) is a disease accompanied by severe liver inflammation. No effective therapy is available yet apart from liver transplantation; therefore, developing novel treatments for ALF is urgently required. Inflammatory mediators released by NF-кB activation play an essential role in ALF. [...] Read more.
Acute liver failure (ALF) is a disease accompanied by severe liver inflammation. No effective therapy is available yet apart from liver transplantation; therefore, developing novel treatments for ALF is urgently required. Inflammatory mediators released by NF-кB activation play an essential role in ALF. Proteasome inhibitors have many medical uses, such as reducing inflammation and NF-кB inhibition, which are believed to account for most of their repurposing effects. This study was undertaken to explore the possible protective effects and the underlying mechanisms of carfilzomib, a proteasome inhibitor, in a mouse model of ALF induced by lipopolysaccharide/D-galactosamine/dimethylsulfoxide (LPS/GalN/DMSO). Carfilzomib dose-dependently protected mice from LPS/GalN/DMSO-induced liver injury, as indicated by the decrease in serum alanine aminotransferase and aspartate aminotransferase levels. LPS/GalN/DMSO increased TNF-α, NF-кB, lipid peroxidation, NO, iNOS, cyclooxygenase-II, myeloperoxidase, and caspase-3 levels. Carfilzomib administration mitigated LPS/GalN/DMSO-induced liver damage by decreasing the elevated levels of TNF-α, NF-кB, lipid peroxidation, nitric oxide, iNOS, cyclooxygenase-II, myeloperoxidase, caspase-3, and histopathological changes. A restored glutathione level was also observed in the carfilzomib-treated LPS/GalN/DMSO mice. Our results demonstrate that carfilzomib protects against LPS/GalN/DMSO-induced ALF by inhibiting NF-кB, decreasing inflammatory mediators, oxidative/nitrosative stress, neutrophil recruitment, and apoptosis, suggesting that carfilzomib may be a potential therapeutic agent for ALF. Full article
(This article belongs to the Special Issue Molecular Insight into Human Diseases: Application of Animal Models)
►▼ Show Figures

Figure 1

13 pages, 1012 KiB  
Article
Dapagliflozin Mitigated Elevated Disomic and Diploid Sperm in a Mouse Model of Diabetes and Recover the Disrupted Ogg1, Parp1, and P53 Gene Expression
by Norah A. Albekairi, Mohammed A. Al-Hamamah, Ali A. Alshamrani, Mohamed S. M. Attia, Ahmed Nadeem, Mushtaq A. Ansari, Sheikh F. Ahmad, Saleh A. Bakheet and Sabry M. Attia
Biomedicines 2023, 11(11), 2980; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11112980 - 6 Nov 2023
Viewed by 809
Abstract
Increases in numerical chromosomal syndromes were observed in children of diabetic mothers. However, the effects of diabetes on male reproduction, specifically numerical chromosomal aberrations (aneuploidy), have not been studied. Furthermore, despite the increasing use of dapagliflozin for diabetes treatment, no data exists on [...] Read more.
Increases in numerical chromosomal syndromes were observed in children of diabetic mothers. However, the effects of diabetes on male reproduction, specifically numerical chromosomal aberrations (aneuploidy), have not been studied. Furthermore, despite the increasing use of dapagliflozin for diabetes treatment, no data exists on its ability to affect aneuploidy levels in germ cells. Thus, our investigation aimed to evaluate the effects of diabetes on spontaneous sperm aneuploidy and whether treatment with dapagliflozin influences the frequency of aneuploidy in the sperm of an experimental diabetic animal model. Our findings show that dapagliflozin has no aneugenic effects on the meiotic stages of spermatogenesis. In contrast, diabetes raised the frequency of aneuploidy, and dapagliflozin administration decreased the elevated levels of disomic and diploid sperm. The level of oxidative stress was markedly increased in diabetic mice, but were reduced by dapagliflozin treatment. Furthermore, the expression of some of DNA repair genes was disrupted in diabetic animals, whereas dapagliflozin therapy restored these disruptions and significantly enhanced DNA repair. Thus, dapagliflozin may effectively ameliorate diabetes-induced aneugenic effects on male meiosis and treating diabetic patients with dapagliflozin may effectively mitigate the transmission of diabetes-induced chromosomal defects to offspring. Full article
(This article belongs to the Special Issue Molecular Insight into Human Diseases: Application of Animal Models)
►▼ Show Figures

Figure 1

Review

Jump to: Research

17 pages, 1401 KiB  
Review
Disease Mechanisms and Therapeutic Approaches in SMARD1—Insights from Animal Models and Cell Models
by Sibylle Jablonka and Ezgi Yildirim
Biomedicines 2024, 12(4), 845; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines12040845 - 11 Apr 2024
Viewed by 531
Abstract
Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a fatal childhood motoneuron disease caused by mutations in the IGHMBP2 gene. It is characterized by muscle weakness, initially affecting the distal extremities due to the degeneration of spinal α-motoneurons, and respiratory distress, [...] Read more.
Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a fatal childhood motoneuron disease caused by mutations in the IGHMBP2 gene. It is characterized by muscle weakness, initially affecting the distal extremities due to the degeneration of spinal α-motoneurons, and respiratory distress, due to the paralysis of the diaphragm. Infantile forms with a severe course of the disease can be distinguished from juvenile forms with a milder course. Mutations in the IGHMBP2 gene have also been found in patients with peripheral neuropathy Charcot–Marie–Tooth type 2S (CMT2S). IGHMBP2 is an ATP-dependent 5′→3′ RNA helicase thought to be involved in translational mechanisms. In recent years, several animal models representing both SMARD1 forms and CMT2S have been generated to initially study disease mechanisms. Later, the models showed very well that both stem cell therapies and the delivery of the human IGHMBP2 cDNA by AAV9 approaches (AAV9-IGHMBP2) can lead to significant improvements in disease symptoms. Therefore, the SMARD1 animal models, in addition to the cellular models, provide an inexhaustible source for obtaining knowledge of disease mechanisms, disease progression at the cellular level, and deeper insights into the development of therapies against SMARD1. Full article
(This article belongs to the Special Issue Molecular Insight into Human Diseases: Application of Animal Models)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop