Intimal hyperplasia is a product of vascular smooth muscle cell proliferation, migration through the internal elastic lamina, and deposition of extracellular matrix proteins driven by growth …
Objective: Endoluminal vascular interventions such as angioplasty initiate a sterile inflammatory response resulting from local tissue damage. This response drives the development of intimal hyperplasia (IH) that, in turn, can lead to arterial occlusion. We hypothesized that the ubiquitous nuclear protein and damage-associated molecular pattern molecule, high-mobility group box 1 …
Intimal hyperplasia model: Surplus saphenous vein samples were longitudinally cut to expose the lumen and further sectioned into ≈1 cm × 1 cm in size. According to sample availability, tissue sections were divided into two groups, i.e., direct method (DM) and scrapping method (SM), and each group was further prepared for 4 different culture ...
The shifted VSMC migration into the intima and the accumulation of extracellular matrix are hallmarks of intimal hyperplasia . Circulating mitogens, such as angiotensin II and plasmin, may be involved in VSMC proliferation and migration owing to overexposure based on endothelial denudation (Fig. 1). Open in a separate window ...
cartilage erosion, synovial hemorrhage scores and intimal hyperplasia in the synovial membrane. 4. 2,3. MSM ... Broken collagen type II fibers. Diseased chondrocyte. Degraded extracellular matrix. In osteoarthritic cartilage the metabolism of chondrocytes get disturbed, causing the slowdown of production of extracellular matrix components and ...
Intimal hyperplasia (IH), a crucial histopathological injury, forms the basis of vascular stenosis and thrombogenesis. In addition, it is common in maladies such as stenosis at the anastomosis of arteriovenous fistula and …
Delayed reendothelialization and intimal hyperplasia (IH) contribute to the failure of vascular interventions. Curcumin (Cur) has been used for various types of diseases with antioxidant, antiproliferative and anti-inflammatory effects. ... in which proteins and organelles are encased in specialized intracellular vesicles and then broken down ...
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The autologous vein remains the standard conduit for lower extremity and coronary artery bypass grafting despite a 30%-50% 5-y failure rate, primarily attributable to intimal hyperplasia (IH) that develops in the midterm period (3-24 mo) of graft maturation. Our group discovered that externally strengthening vein grafts by cross-linking the adventitial collagen with photochemical tissue ...
Introduction. Intimal hyperplasia (IH) is a buildup of myofibroblast-like cells (neointimal cells) and extracellular matrix (ECM) within the tunica intima, the innermost layer of the vein ().In preaccess veins of patients with CKD, IH manifests as an idiopathic and benign histologic feature that does not compromise blood flow (2 –6).After arteriovenous fistula (AVF) …
The underlying pathophysiology of venous graft disease and late bypass failure includes intimal hyperplasia and subsequent accelerated atherosclerosis. 3 More than 100 …
Home Publications Departments. Prevention of intimal hyperplasia after balloon angioplasty and / or stent insertion. or How to mend a broken heart - Just say NO. Mark; Harnek, Jan
Neointimal hyperplasia is a physiologic healing response to injury to the blood vessel wall, involving all the three arterial layers and it occurs in the presence of internal (endovascular) or external (surgical) injury. ... There are known risk factors for Intimal Hyperplasia, such as diabetes, gender, presence of systemic inflammation ...
In coronary arteries the development of intimal hyperplasia can be significantly reduced with site-specific delivery of nitric oxide donor. The pathway for this effect is cGMP dependent.
Coronary artery bypass grafting (CABG) is an effective treatment for coronary heart disease, with vascular transplantation as the key procedure. Intimal hyperplasia (IH) gradually leads to vascular stenosis, seriously affecting the curative effect of CABG. Mesenchymal stem cells (MSCs) were used to alleviate IH, but the effect was not satisfactory.
enlargement of alveolar airspaces caused by destruction of septae w/ fibrosis afterwards appears: dilated alvoli, destruction to structural support to lymphatic vessels produces heavy pigment deposition in the tissue microscopic findings: enlarged, round airspaces with club like ends of broken septae sticking into alveoli, scant clear mucoid sputum, quiet chest
Intimal hyperplasia (IH) remains a major cause of poor patient outcomes after surgical revascularization to treat atherosclerosis. A multitude of drugs have been shown to prevent the development of IH. Moreover, endovascular drug delivery following angioplasty and stenting has been achieved with a marked diminution in the incidence of restenosis.
A direct role of TNF-α in inducing reactive oxygen species (ROS) in cellular events that promote intimal hyperplasia was also evident. In vivo studies in TNF-α-knockout mice showed improved cardiac functions and decreased ROS production . The oxidative damage from ROS was found to alter many cellular functions, including VSMC migration, and a ...
By definition, intimal hyperplasia is an abnormal accumulation of cells in the vascular tunica intima; the cell number is increased because of proliferation and/or migration of vascular wall cells, predominantly smooth muscle cells, often in response to a traumatic stimulus.1 Whereas endothelial denudation is an important injury, especially in surgical procedures,2 the absence …
Postoperative intimal hyperplasia is the major cause of the vein graft occlusion. It is very important to establish an animal model for the start of research. After my vascular surgery residency in Japan, I started my research work on postoperative intimal hyperplasia at the University of Wisconsin- …
Phenotypic shift of vascular smooth muscle cells (VSMCs) plays a key role in intimal hyperplasia, especially in patients with diabetes mellitus (DM). This study aimed to investigate the role of dynamin-related protein 1 (DRP1) in mitochondrial fission-mediated VSMC phenotypic shift and to clarify wh …
Variability in intimal hyperplasia in preaccess basilic veins from patients with ESKD. (A–C) Cross-sections of basilic veins collected during first-stage surgery of a two-stage …
Intimal hyperplasia is thought to play a critical role in the development of restenosis after percutaneous transluminal coronary angioplasty and in the progression of atherosclerosis. Induction of M3 expression resulted in a 67% reduction in intimal area and a 68% reduction in intimal/medial ratio after femoral artery injury. These data support ...
By definition, intimal hyperplasia is an abnormal accumulation of cells in the vascular tunica intima; the cell number is increased because of proliferation and/or migration of vascular wall …
The pathophysiology of intimal hyperplasia. Native blood vessel walls are made of three layers: tunica externa, tunica media, and tunica intima. 21 Tunica externa is the acellular outermost layer composed of collagenous fibers and elastic fibers, and tunica media is the …
Despite the many recent technological advances in vascular intervention, intimal hyperplasia (IH) remains an expensive, morbid, and unsolved problem. It is estimated that hyperplastic …
Intimal Hyperplasia. The process of intimal hyperplasia is common to various forms of vascular diseases, such as atherosclerosis, restenosis, and transplant vasculopathy. …
The vascular access remains the lifeline for the hemodialysis patient. The most common etiology of vascular access dysfunction is venous stenosis at the vein-artery anastomosis in arteriovenous fistula and at the vein-graft anastomosis …
Symptomatic recurrent carotid disease occurs in 0.6% to 3% (mean, 1.2%) of patients after carotid endarterectomy.1 Asymptomatic recurrent disease occurs with a much greater frequency, which varies widely (6.7% to 21%), depending on the noninvasive method of detection used.2 These figures represent absolute recurrence rates within variable periods of time after …
Low flow promotes instent intimal hyperplasia: Comparison with lumen loss in balloon-injured and uninjured vessels and the effects of the antioxidant pyrrolidine dithiocarbamate. ... [IEL] intact, 1 = IEL broken media compressed but not lacerated, 2 = media lacerated, EEL intact, 3 = EEL lacerated; injury then averaged per segment) [13]. ...
The most commonly used procedures to induce arterial injury in mice are carotid artery ligation with cessation of blood flow and mechanically-induced denudation of endothelium in the carotid or the femoral arteries. Both procedures result in neointimal hyperplasia after …
Aims: Cyclooxygenase-2-derived prostaglandin E2 (PGE2) is thought to promote vascular intimal hyperplasia (IH). It has been reported that the PGE2 receptor EP4 is upregulated in injured vessels, and that EP4 signaling in vascular smooth muscle cells (VSMCs) promotes IH. In contrast, EP4 in endothelial cells has been demonstrated to restrain IH.
The intima-to-media (I/M) ratio was calculated as the intimal area divided by the media area. Arteries with a broken IEL or thrombosis by CME stain were excluded from the study. ... Intimal hyperplasia is defined as the formation of a neointimal layer within the internal elastic lamina (arrows). B, Average intimal areas of injured WT and KO ...
Intimal hyperplasia is a normal adaptive feature of arteries in response to injuries, which include invasive vascular interventions. Its development limits the long-term success of bypass grafts. Various pharmacological agents have been successfully employed in experimental models to reduce the degree of intimal hyperplasia.
Objectives: Intimal hyperplasia is a serious clinical problem associated with the failure of therapeutic methods in multiple atherosclerosis-related coronary heart diseases, which are initiated and aggravated by the polarization of infiltrating macrophages. The present study aimed to determine the effect and underlying mechanism by which tumor necrosis factor receptor …
We determined whether a novel biodegradable external mesh stent could inhibit medial-intimal hyperplasia by suppressing hemodynamic stress on vein grafts and improve long-term patency. Methods: Twenty-four beagles underwent bilateral femoral interposition grafting using reversed femoral veins. Vein grafts were externally supported by a novel ...