Atrial fibrillation (AF) is the most common sustained arrhythmia and cardiac fibrosis is a major component in driving its progressive nature. Quantitative histological assessment of fibrosis in animal models is crucial for understanding AF, but current published studies present various methodologies that limit comparison. This systematic review examines 195 AF studies across multiple animal models (mice, rats, goats, dogs, pigs and horses) to summarize: 1) quantified fibrosis results, 2) methodologies for histological fibrosis assessment and 3) evaluate anti-fibrotic therapies used in these studies. The fibrosis quantified across the studies ranged from 0.34% to 60.2% depending on the animal, intervention model and quantification method. The findings underscore the need for a standardized fibrosis quantification protocol in AF research, enabling comparison across studies and offering greater insight into potential pharmacological interventions.
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http://dx.doi.org/10.1016/j.hrthm.2025.03.1880 | DOI Listing |
Mol Pharm
March 2025
Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Positive surgical margins following radical prostatectomy significantly contribute to tumor recurrence. While systemic chemotherapy demonstrates limited efficacy in this context, local chemotherapy drug delivery systems based on nanomaterials offer promising strategies to address this issue by modifying drug release kinetics and distribution, thereby enhancing antitumor effects while minimizing the toxicities associated with systemic chemotherapy. In this study, we utilized electrospun nanofibrous mats loaded with docetaxel for sustained drug delivery.
View Article and Find Full Text PDFPLoS One
March 2025
Department of Orthopaedics, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, Shanxi, China.
Purpose: This study aimed to examine the differential expression profiles of plasma metabolites in rat models of post-traumatic osteoarthritis (PTOA) and elucidate the roles of metabolites and their pathways in the progression of PTOA using bioinformatics analysis.
Method: Plasma samples were collected from 24 SD female rats to model PTOA, and metabolomic assays were conducted. The samples were divided into three groups: the surgically induced mild PTOA group (Group A: 3 weeks postoperative using the modified Hulth model; age 2 months), the surgically induced severe PTOA group (Group B: 5 weeks postoperative using the modified Hulth model; age 2 months), and the normal control group (Group C: healthy rats aged 2 months).
J Immunol
January 2025
Department of Biological Sciences, California State University San Marcos, San Marcos, CA, United States.
Obesity is associated with comorbidities including type 2 diabetes, chronic nonhealing wounds, and psoriasis. Normally, skin homeostasis and repair is regulated through the production of cytokines and growth factors derived from skin-resident cells including epidermal γδ T cells. However, epidermal γδ T cells exhibit reduced proliferation and defective growth factor and cytokine production during obesity and type 2 diabetes.
View Article and Find Full Text PDFJ Immunol
January 2025
Institute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Taipei City, Taiwan.
Decoy receptor 3 (DcR3), a soluble receptor in the tumor necrosis factor receptor superfamily, regulates the functions of monocytes, macrophages, dendritic cells, and T cells. Previous studies have demonstrated that DcR3 suppresses B cell proliferation in vitro and ameliorates autoimmune diseases in animal models; however, whether and how DcR3 regulates antibody production is unclear. Using a DcR3 transgenic mouse model, we found that DcR3 impaired the T cell-dependent antigen-stimulated antibody response.
View Article and Find Full Text PDFJ Immunol
February 2025
Orthopedics Department, Central Hospital of Ezhou, Ezhou, China.
Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β.
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