Graft Dysfunction Model
Graft Dysfunction Model - Related Videos
07:37
Mouse Models for Graft Arteriosclerosis
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Cited by 17 •
2013
We describe protocols for our mouse graft arteriosclerois (GA) models which involve interposition of a mouse vessel segment into a recipient of the same inbred strain. By backcrossing additional genetic changes into the vessel donor, the model can assess the effect of specific genes on GA.
02:34
Modeling Preservation Injury in Porcine Donor Kidney: A Procedure to Induce Graft Dysfunction by Subjecting Kidney to Prolonged Cold Ischemia
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2025
In this video, we describe a technique to induce preservation injury via the prolonged cold ischemic storage time in porcine donor kidney.
03:35
A Technique for Human Skin Grafting in a Mouse Model
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2025
This video demonstrates a method for grafting human skin onto an immunodeficient mouse with a suppressed neutrophil response. The method involves applying human split-thickness skin to the mouse's graft bed, sealing it, and covering it for recovery. Eventually, the human skin adheres to the mouse's skin, establishing vascularization and circulation, resulting in a successful skin xenograft.
06:26
Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
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Cited by 1 •
2025
Mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD) with metabolic dysfunction, hepatic gene expression changes, and liver histopathological alterations that resemble human MASLD, including fibrosis that progresses to advanced fibrosis stage 3. This model can be used in studies of MASLD pathophysiology and in pre-clinical studies of new therapies.
12:39
Implantation of Inferior Vena Cava Interposition Graft in Mouse Model
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Cited by 24 •
2014
To improve our knowledge of cellular and molecular neotissue formation, a murine model of the TEVG was recently developed. The grafts were implanted as infrarenal vena cava interposition grafts in C57BL/6 mice. This model achieves similar results to those achieved in our clinical investigation, but over a far shortened time-course.
FAQs
Ischemia-reperfusion injury is an early damaging process examined in graft dysfunction models. Reduced blood supply followed by restored circulation can affect graft cells and blood vessels, creating conditions associated with inflammation and oxidative stress. Studying this sequence helps researchers separate early post-transplant injury from later processes and assess whether protective interventions preserve graft structure and function.
Immune recognition helps explain how transplanted tissue can become a target of damaging responses. In experimental analysis, researchers examine immune responses alongside tissue structure and graft function rather than treating dysfunction as a single event. This comparison supports distinction between early injury and chronic rejection, allowing investigations to connect immune activity with progressive functional decline.
Oxidative stress can contribute to injury in graft cells and blood vessels, while progressive fibrosis represents a longer-term structural change associated with declining graft performance. A graft dysfunction model can examine these mechanisms together with inflammation and immune responses. Their interaction helps researchers investigate how initial damage may develop into persistent tissue remodeling and chronic dysfunction.
Evaluation combines structural, immunological, and functional measurements. Structural analysis identifies tissue or vascular changes, immune assessment characterizes relevant responses, and functional measurements indicate whether the graft is losing performance. Considering these readouts together helps researchers determine whether observed dysfunction reflects early injury, chronic rejection, or progressive damage rather than relying on a single indicator.
Researchers can compare measurable immune responses, structural alterations, and functional decline across stages of graft injury. Patterns that accompany worsening performance may help identify candidate biomarkers associated with graft dysfunction or chronic rejection. Such markers could improve experimental monitoring and clarify relationships between tissue damage, vascular changes, and the loss of graft function.
These models provide a controlled way to examine strategies intended to protect transplanted tissues or organs before broader evaluation. Investigators can relate an intervention to changes in graft structure, immune responses, and function while considering mechanisms such as inflammation, oxidative stress, or fibrosis. The resulting evidence can inform approaches to improve graft survival and guide transplant biology research.