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Biomedicines
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Animal Models for the Study of Human Diseases
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Animal Models for the Study of Human Diseases

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3801

Special Issue Editor

Dr. Yong-He Ding

E-Mail Website
Guest Editor
1. Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA
2. The Biomedical Sciences Institute, Qingdao University, Qingdao 266073, China
Interests: genetics; cardiomyopathy; cardiac conduction diseases; zebrafish; turquoise killifish

Special Issue Information

Dear Colleagues,

The use of animal models in biomedical research has been instrumental in advancing our understanding of human diseases. Animal models allow researchers to simulate the pathophysiology of human conditions, providing critical insights into disease mechanisms, therapeutic interventions, and drug efficacy. The translation of basic scientific knowledge into clinical applications often relies on these models, which provide important preclinical data to inform clinical trials and treatment strategies.

This Special Issue, titled "Animal Models for the Study of Human Diseases", aims at showcasing the latest advancements in the use of animal models for understanding human diseases, improving therapeutic approaches, and bridging the gap between basic science and clinical practice. We invite high-quality research papers and reviews that highlight innovative techniques, findings, and applications in this ever-evolving field.

For this Special Issue, we encourage submissions on a wide array of topics related to animal models for human diseases, including, but not limited to, the following:

1. Development and improvement of animal models for specific human diseases:

  • Creation of novel animal models for diseases.
  • Development or advancements in more accurate models to reflect human disease heterogeneity and complexities.
  • Genetic, environmental, and mechanistic factors in animal models of human disease.

2. Modeling disease progression and treatment responses:

  • Animal models for studying disease progression, biomarkers, and the molecular basis of disease.
  • Use of animal models for testing drug efficacy, safety, and toxicity.
  • Evaluation of therapeutic strategies, including gene therapy, stem cell therapy, immunotherapy, and small molecule treatments.

3. Humanization of animal models:

  • Generation of humanized animal models to better mimic human physiology and pathology.
  • Development of transgenic animals to study human diseases at the molecular and cellular levels.
  • Integration of human tissues or cells into animal models to better reflect human disease and treatment responses.

4. Translational applications of animal models:

  • From bench to bedside: the role of animal models in advancing clinical treatments and therapies.
  • Impact of animal research on personalized medicine, including the use of animal models to identify patient subtypes or predict treatment responses.
  • Animal models in the study of rare diseases and orphan drug development.

Dr. Yong-He Ding
Guest Editor

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 models
  • zebrafish
  • mice
  • rats

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Published Papers (4 papers)

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Research

25 pages, 2547 KB  
Article
Mechanically Induced Pulpitis: A Rat Model That Preserves Animal Well-Being
by María Alexandra Bedoya, Gloria Cristina Moreno, Camilo Durán, Adriana Camacho, Angel Eduardo Pirela, Stefany Rojas Lozano, Maddy Mejía, Eddy Herrera, Luz-Stella Rodríguez Camacho, Lorenza Jaramillo and Nelly S. Roa
Biomedicines 2025, 13(8), 1925; https://doi.org/10.3390/biomedicines13081925 - 7 Aug 2025
Viewed by 449
Abstract
Background: Understanding the mechanisms underlying dental pain caused by pulpitis in humans has led to the development of animal models, such as the rat, which enable the study of the mechanisms underlying inflammation; the use of these models is considered ethically justified [...] Read more.
Background: Understanding the mechanisms underlying dental pain caused by pulpitis in humans has led to the development of animal models, such as the rat, which enable the study of the mechanisms underlying inflammation; the use of these models is considered ethically justified when the anticipated scientific benefits outweigh the potential impacts on animals in the harm/benefit balance. Objective: To develop a rat model of mechanically induced pulpitis and to evaluate the potential impact on animal well-being. Methods: Pulpitis was mechanically induced in male Lewis rats (13–16 weeks, 350–400 g) which were anesthetized and endotracheally intubated. Following pulp exposure, the cavity was sealed with either amalgam (n = 10) or zinc phosphate cement (n = 10). Following recovery and return to their housing, behavioral assessments and histological evaluations using Hematoxylin and Eosin (H&E) staining were conducted in separate cohorts at two time points: 3 h and 5 days following the procedure. Results: A standardized model of mechanically induced pulpitis was established and verified clinically and by histopathological analysis, which showed evidence of the inflammatory process and revealed no statistically significant differences in the scoring of pain, discomfort, or distress, nor in the measurements of food and water consumption or body weight. Conclusions: The behavioral assessments conducted in this study supported the implementation of a safe and easily reproducible model for future research aimed at elucidating the mechanisms underlying pulp inflammation. Full article
(This article belongs to the Special Issue Animal Models for the Study of Human Diseases)
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13 pages, 1589 KB  
Article
CRISPR/Cas9 Reduces Viral Load in a BALB/c Mouse Model of Ocular Herpes Infection
by Luiza Silveira Garcia, Rafaela Moraes Pereira de Sousa, Viviane Souza Campos, Erik Machado Ferreira, Cynthia Machado Cascabulho, Elen Mello de Souza and Vanessa Salete de Paula
Biomedicines 2025, 13(7), 1738; https://doi.org/10.3390/biomedicines13071738 - 16 Jul 2025
Viewed by 592
Abstract
Background/Objectives: Simplexvirus humanalpha1 (HSV-1) can cause herpetic keratitis, which is the most common cause of infectious blindness in developed countries. Some patients can develop toxicity or resistance to available treatments and may require keratoplasty. Methods: As an alternative therapy, the CRISPR/Cas9 anti-HSV-1 [...] Read more.
Background/Objectives: Simplexvirus humanalpha1 (HSV-1) can cause herpetic keratitis, which is the most common cause of infectious blindness in developed countries. Some patients can develop toxicity or resistance to available treatments and may require keratoplasty. Methods: As an alternative therapy, the CRISPR/Cas9 anti-HSV-1 activity was assessed in an experimental model of BALB/c mice. Results: The results showed that the viral load in the eyes of mice inoculated with HSV-1 at 107 PFU/mL was 4.5 ± 0.2 log10 copies/mL. In contrast, mice inoculated with 109 PFU/mL exhibited a high viral load of 8.1 ± 0.4 log10 copies/mL. The detection of HSV-1 DNA and lesions in the eye was consistent with the viral inoculum of the infection. Next, antiviral activity showed that 200 ng/µL of CRISPR/Cas9 reduced the viral load by 2 logs (p ≤ 0.0001), as well as the lesion scores, compared to the untreated group. Conclusions: Together, the data suggest that CRISPR/Cas9 could be investigated as an alternative therapy for ocular herpes. Full article
(This article belongs to the Special Issue Animal Models for the Study of Human Diseases)
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15 pages, 3629 KB  
Article
The Modified Canine Groove Model of Osteoarthritis
by Goran S. van der Weiden, Björn P. Meij, Amy van de Belt, Roel J. H. Custers, Sanne K. Both, Marcel Karperien and Simon C. Mastbergen
Biomedicines 2025, 13(4), 913; https://doi.org/10.3390/biomedicines13040913 - 9 Apr 2025
Viewed by 506
Abstract
Background/Objectives: In the original canine groove model of osteoarthritis (OA), superficial scratches to the cartilage lead to slow progressive cartilage damage, with inflammation mimicking key aspects of human disease. The present study assesses a modified canine groove model with full-thickness cartilage grooves, [...] Read more.
Background/Objectives: In the original canine groove model of osteoarthritis (OA), superficial scratches to the cartilage lead to slow progressive cartilage damage, with inflammation mimicking key aspects of human disease. The present study assesses a modified canine groove model with full-thickness cartilage grooves, gouged with a 3-mm biopsy punch, in the femoral condyles. This modified model enables the study of cartilage repair techniques, such as scaffold implantation. Methods: Cartilage defects were induced in the right knee of five mongrel dogs (four females, one male; 17 ± 4 months; 25.9 ± 2.0 kg) using the modified groove model, creating two full-thickness cartilage grooves on the femoral condyles. Data of a previously studied cohort of nine dogs (nine females; 18 ± 6 months; 17.6 ± 0.7 kg) with OA induced according to the original groove model served as the canine OA standard. Both groups were monitored up to 45 weeks post-surgery. Pain/function was assessed by force plate analysis, and cartilage integrity, chondrocyte activity, and synovial inflammation were evaluated on the surgically untouched tibial plateaus by macroscopic, histologic, and biochemical analyses. Results: Force plate analysis showed no significant changes in either group. Both models exhibited OA features. Experimental knees had more macroscopic and histologic damage, reduced proteoglycan content, and impaired retention of proteoglycans than controls. The modified groove model had less severe cartilage damage and synovial inflammation (p = 0.026, p = 0.017), with no other significant differences. Conclusions: The modified groove model induces OA at a slow pace, mirroring post-traumatic OA development in humans. It represents a mild OA model, comparable to the original groove model, and may be useful for evaluating cartilage repair strategies, such as scaffold implantation. Full article
(This article belongs to the Special Issue Animal Models for the Study of Human Diseases)
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17 pages, 12389 KB  
Article
Highlighting the Role of Prenatally Administered Drugs in the Production of Dental Enamel Defects in Rats by Polarized Light Microscopy
by Mihai Popescu, Marilena Bătăiosu, Stelian-Mihai-Sever Petrescu, Mihaela Ionescu, Marius Ciprian Văruț, Diana Elena Vlăduțu, Tiberius-Cătălin Dudan, Adina-Monica Chiriac, Camelia Fiera (Maglaviceanu) and Veronica Mercuț
Biomedicines 2025, 13(3), 575; https://doi.org/10.3390/biomedicines13030575 - 25 Feb 2025
Viewed by 1849
Abstract
Background/Objectives: Although factors acting both prenatally and postnatally are taken into consideration, the etiopathogenesis of developmental defects of enamel (DDE) is not fully understood. Among the medications used for a variety of ailments, amoxicillin and cefaclor are indicated as having a part in [...] Read more.
Background/Objectives: Although factors acting both prenatally and postnatally are taken into consideration, the etiopathogenesis of developmental defects of enamel (DDE) is not fully understood. Among the medications used for a variety of ailments, amoxicillin and cefaclor are indicated as having a part in the development of DDE. The objective of the present study was to reproduce DDE in the laboratory in rats by administering amoxicillin, ibuprofen, and cefaclor. These lesions were subsequently diagnosed using polarized light microscopy (PLM). Methods: This study was conducted on Wistar rats, which were given prenatally drugs possibly involved in the production of DDE. After macroscopic examination and identification of enamel defects, bright-field microscopy (BFM) and PLM examination were performed. Results: The group that received cefaclor was the most affected, according to the data gathered from this study. This group was followed by the groups that received amoxicillin in a double dose, ibuprofen, amoxicillin in a standard dose, and the control group. Conclusions: In the control group, DDE was identified in a reduced number, resulting in the fact that there are other factors involved, besides the drugs administered, in the development of DDE. Following this research, it was concluded that DDE in the form of demineralization was more frequently recorded in the cefaclor and ibuprofen groups, while DDE in the form of hypoplasia was more frequently recorded in the double-dose and standard-dose amoxicillin groups. Full article
(This article belongs to the Special Issue Animal Models for the Study of Human Diseases)
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