Intimal Hyperplasia
Intimal Hyperplasia - Related Videos
04:33
Carotid Artery and Jugular Vein Interposition: A Technique to Induce Venous Intimal Hyperplasia in Rabbit Model
0 Views •
2025
This video demonstrates the interposition of the rabbit carotid artery with the jugular vein to induce venous intimal hyperplasia by subjecting the veins to arterial pressure. This model will help investigate molecular and genetic interventions to attenuate the progression of intimal hyperplasia after revascularization surgeries.
08:34
Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models
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Cited by 8 •
2014
This video shows two models of intimal plaque development in murine arteries and emphasizes the differences in myointimal hyperplasia and atherosclerosis.
07:02
A Rabbit Venous Interposition Model Mimicking Revascularization Surgery using Vein Grafts to Assess Intimal Hyperplasia under Arterial Blood Pressure
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Cited by 3 •
2020
The present protocol aims to experimentally create venous intimal hyperplasia by subjecting veins to arterial blood pressure for developing strategies to attenuate venous intimal hyperplasia following revascularization surgery using vein grafts.
01:26
Cellular Adaptation III: Hyperplasia
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2026
Hyperplasia is an increase in the number of cells in a tissue or organ due to enhanced cell division. It is an adaptive, controlled response to stimuli such as injury, hormones, or stress, involving mitosis to produce genetically identical cells and support tissue repair and regeneration.Tissue CapacityCertain tissues, including the epidermis, intestinal epithelium, bone marrow, and fibroblasts, have a high potential for hyperplasia. Others, such as bone, cartilage, and smooth muscle, show...
08:38
Renal Capsule Xenografting and Subcutaneous Pellet Implantation for the Evaluation of Prostate Carcinogenesis and Benign Prostatic Hyperplasia
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Cited by 13 •
2013
We describe the manufacture of compressed hormone pellets, as well as subcutaneous surgical implantation into mice. This strategy can be combined with the growth of cell and tissue xenografts under the renal capsule of athymic nude mice to evaluate hormonal carcinogenesis and regulation of benign prostate growth.
FAQs
After endothelial injury, inflammatory signals and altered blood flow stimulate vascular smooth muscle cells to leave the media and enter the intima. These cells then proliferate and produce extracellular matrix, which expands the neointimal lesion. This coordinated cellular response helps explain how a previously treated or injured vessel can progressively lose lumen space.
Both factors provide stimuli that change the vessel’s response after injury. Inflammatory signals promote cellular activity, while altered blood flow contributes to the conditions that encourage vascular smooth muscle cell migration and proliferation. Their combined influence connects the original endothelial disruption with extracellular matrix accumulation and subsequent neointimal growth.
Extracellular matrix production increases the material within the developing neointimal lesion after vascular smooth muscle cells migrate and proliferate. As this lesion enlarges, it contributes to thickening of the vessel wall and reduction of the lumen. This mechanism shows why intimal hyperplasia reflects abnormal remodeling rather than cellular proliferation alone.
Vascular intervention can injure the endothelium and initiate the inflammatory and flow-related responses associated with intimal hyperplasia. Smooth muscle cell migration, proliferation, and extracellular matrix production may then create a neointimal lesion inside the treated vessel. If the lesion narrows the lumen, the vessel can develop restenosis, meaning recurrent narrowing after treatment.
The process is a recognized contributor to failure of vascular grafts and fistulas. Injury or altered vascular conditions can stimulate neointimal lesion formation, which may narrow the lumen and compromise the treated vascular connection. Studying these changes helps clinicians and researchers interpret why a graft or fistula may not remain functionally effective over time.
Understanding the cellular and inflammatory mechanisms directs research toward approaches that limit abnormal remodeling. Investigated strategies include drug-coated devices, anti-inflammatory treatments, and therapies designed to restrict the migration or proliferation response associated with lesion formation. These approaches are relevant to restenosis prevention and to improving the durability of vascular interventions, grafts, and fistulas.