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Fascia and the Circulatory System
Published in David Lesondak, Angeli Maun Akey, Fascia, Function, and Medical Applications, 2020
Anita Boser, Kirstin Schumaker
Far from being inert, as previously assumed, current research suggests that the adventitia has a dynamic effect on the tunica media and endothelium, including the size of the lumen. Immune cells and progenitor cells reside in the adventitia, providing protection and repair for the vessels and possibly also the surrounding tissues.6 Stenmark et al. describes the adventitia as a “biologic processing center” that may be the first to react to vessel injury.7 Surrounding tissues also affect arteries through the adventitia. The cells of the adventitia respond to mechanical tension transmitted through the fibrous matrix around the vessels. Connective tissue fibers connect to nitric oxide receptors in arterioles and send signals that create vessel dilation in response to muscular contraction.8
Synthetic DNA-Based Compounds for the Prevention of Coronary Restenosis: Current Status and Future Challenges
Published in Eric Wickstrom, Clinical Trials of Genetic Therapy with Antisense DNA and DNA Vectors, 2020
Andrew Zalewski, Yi Shi, John D. Mannion, Femando Roqué
Experimentally, adventitial cell proliferation, neointimal formation and remodeling changes are clearly linked to the severity of vascular injury (Shi et al., 1996b), which raises the question whether such findings are applicable to the clinical setting. Although not appreciated angiographically, the adventitia is often exposed to the lumen after balloon angioplasty or other procedures in patients (e.g., stent implantation, atherectomy), setting conditions that promote fibroblast activation and the ensuing events leading to restenosis (Kohchi et al., 1987; den Heijer et al., 1994; Colombo et al., 1995).
Renal Pathophysiology
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Herman S. Fernando, Mohamed Yehia Abdallah, Iqbal S. Shergill
Regarding retroperitoneal fibrosis (RPF), which of the following is FALSE?One possible pathogenesis could be the development of vasculitis in the adventitial vessels of the aorta and periaortic small vessels.Inflammatory bowel disease (IBD) is reported to be a cause of RPF.The classic radiologic findings include medial deviation of extrinsically compressed ureters with hydronephrosis.CT typically reveals a well demarcated retroperitoneal mass, isodense to muscle on unenhanced studies.Tamoxifen, a steroidal anti-oestrogen, has also been used for primary treatment at a dose of 20 mg per day with a reported response rate of 80%.
Nuclear receptor subfamily 1 group D member 1 suppresses the proliferation, migration of adventitial fibroblasts, and vascular intimal hyperplasia via mammalian target of rapamycin complex 1/β-catenin pathway
Published in Clinical and Experimental Hypertension, 2023
Ke Peng, Mingliang Wang, Jun Wang, Qiang Wang, De Li, Xiongshan Sun, Yongjian Yang, Dachun Yang
Intimal hyperplasia is a crucial process for ISR (5). Adventitia, an important part of the vascular wall, serves as an active participant in the vascular diseases (30). Recent research showed that AFs, the main component of vascular adventitia, were involved in intimal hyperplasia and vascular remodeling (30,31). Nevertheless, the underlying mechanisms are largely unknown. Our current study demonstrates that NR1D1 suppresses the proliferation and migration of AFs. NR1D1-mediated regulation of AFs depends on the downregulation of β-catenin and mTORC1. Inhibition of β-catenin by NR1D1 relies on the decreased activity of mTORC1. Importantly, NR1D1 also suppresses the early-stage proliferation of AFs within adventitia and subsequent intimal hyperplasia. Therefore, our data highlight a crucial role of NR1D1 in the treatment of intimal hyperplasia-associated vascular diseases.
Targeting VCAM-1: a therapeutic opportunity for vascular damage
Published in Expert Opinion on Therapeutic Targets, 2023
Mayarling F Troncoso, Magda C Díaz-Vesga, Fernanda Sanhueza-Olivares, Jaime A Riquelme, Marioly Müller, Luis Garrido, Luigi Gabrielli, Mario Chiong, Ramon Corbalan, Pablo F Castro, Sergio Lavandero
The cardiovascular system includes the heart and blood vessels that pump and deliver blood throughout the body. Blood vessels are structured in three layers: the tunica intima, media, and adventitia. The tunica intima, or inner layer, comprises endothelial cells (EC) in contact with the blood. The tunica media or medial layer is formed mainly by vascular smooth muscle cells (VSMC) and the extracellular matrix, such as collagen and elastin, that regulates vascular tone and the integrity of vessels. In capillaries, the medial layer does not contain VSMC, but pericytes form a thin wall that facilitates the transport of blood components [3]. The adventitia layer, or outer layer, comprises fibroblasts, nerves, and small arteries (Vasa vasorum) that deliver nutrients to this layer [4].
Interdisciplinary management of peripheral arteriovenous malformations: review of the literature and current proceedings
Published in Journal of Plastic Surgery and Hand Surgery, 2022
Felix F. Strübing, Stefan Porubsky, Amir K. Bigdeli, Volker J. Schmidt, Lena Krebs, U. Kneser, Maliha Sadick
Histologically, AVMs represent abnormal direct connections between arteries and veins skipping the organ-specific capillary bed. These abnormal arterio-venous communications consist of arterioles, capillaries, and venules haphazardly aggregated into vascular clusters. Abrupt dilation and changes in the vessel wall thickness or structure are typical findings. The veins often show reactive intimal hyperplasia. The adventitia and the adjacent connective tissue are fibrosed (Figures 4(D–F) and 7(G)). Depending on the localization and patient history, the lesions may show hemorrhage, necrosis and ulceration of the skin or mucosa. The pathologist is commonly confronted with the differential diagnosis of hemangiomas. In contrast to AVMs, hemangiomas typically lack arterial and arteriolar structures and intralesional nerve fibers [19]. Clinically, hemangiomas would present as solid, bright red, hypervascularized tumors, densely packed with blood vessels. Histopathologically, they show positivity for GLUT-1 in their endothelium [20].