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General Radiation Histopathology
Published in George W. Casarett, Radiation Histopathology, 2019
A factor of importance in the resistance or susceptibility of irradiated tissues and organs to the development of delayed radiation-induced lesions of serious clinical significance is the ability retained by the irradiated fine vasculature to regenerate and remodel under conditions of added injury or stress. Additional injury or stress that is either so mild or so localized as to require no extensive vascular remodeling may be adequately resisted or repaired. However, more marked or more diffuse injury or stress such as might result from diffuse infection and inflammation (which may require for repair a marked generalized hyperemia and considerable vascular remodeling without hinderance of the ability of the vascular endothelium by an increased fibrillar connective tissue barrier) may not be adequtely resisted or repaired, and necrosis may result. Infection or diffuse trauma of irradiated organs in which the fine vasculature has been reduced and in which regeneration of the fine vasculature is inhibited by an increase in the histohematic fibrous barrier is often a precipitating factor in delayed radionecrosis of such organs. Delayed radionecrosis resulting at least partly from such complications may occur at any time, depending upon the degree of devitalization of the supporting tissues at any particular time, which in turn depends upon dose.
Wound healing angiogenesis: An overview on mathematical models
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
A.C. Guerra, J. Belinha, R.M. Natal Jorge
Several other authors used PDEs and the same parameters analysed by Pettet et al. (1996) to model angiogenesis with different levels of complexity (Byrne et al. 2000, Maggelakis 2003, Schugart et al. 2008, Flegg et al. 2010). Byrne et al. (2000) included in the model the effect of vascular remodelling. Maggelakis (2003) studied the effect of the oxygen concentration through the wound space and the production, depletion and absorption of macrophage derived growth factors (MDGFs). Schugart et al. (2008) studied for the first time the effect of tissue oxygen tension on cutaneous wound healing. This model also incorporated more variables, such as capillary sprouts, inflammatory cells (macrophages and neutrophils), fibroblasts and extracellular matrix (ECM) density. Flegg et al. (2010) studied for the first time the role of hyperbaric oxygen therapy in the healing process. The model described the interactions in space and time of oxygen and chemo-attractant concentrations, and the densities of capillary tip, blood vessel, fibroblast and ECM.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
Vascular remodeling is a general term for the process of structural changes that can happen during or after vessel formation as a part of vasculogenesis, angiogenesis, or arteriogenesis. These structural changes may include changes in size, shape, composition, maturation, or specification of vessel type toward vein or artery. Remodeling can take place in an individual vessel or a whole network, with some vessels becoming stabilized or strengthened and some vessels regressed or pruned.
Qiqilian ameliorates vascular endothelial dysfunction by inhibiting NLRP3-ASC inflammasome activation in vivo and in vitro
Published in Pharmaceutical Biology, 2023
Yuan Luo, Zhenyuan Tan, Yun Ye, Xiaocong Ma, Guihua Yue
Hypertension is a prevalent cardiovascular disease. Globally, the number of patients with hypertension aged 30–79 has doubled to 1.28 billion since 1990 (NCD-RisC 2021). In patients with hypertension, the continuous increase in arterial pressure damages the blood vessels and impairs the function of many target organs, including the heart, kidneys, and brain, eventually increasing the risk of diseases such as cardiac hypertrophy, cerebral hemorrhage, and atherosclerosis. High blood pressure causes a longer disease course and substantial harm, making it a leading cause of premature death worldwide. The vascular endothelium is the largest endocrine and paracrine organ with crucial and diverse physiological functions. The dysfunction of vascular endothelium owing to organic damage may result in the onset and progression of hypertension. Furthermore, hypertension can cause endothelial damage, thus creating a vicious cycle. Vascular remodelling refers to the adaptive functional and structural alterations that occur in blood vessels in response to the changes in the internal and external environment (Baumbach and Heistad 1989). Vascular remodeling-related disease is regulated by the renin–angiotensin system, inflammatory response, and redox regulation (Whiteford et al. 2016). As a chronic inflammatory condition, the onset and progression of hypertension are also associated with immune hyperactivation and the release of inflammatory mediators in vivo (Vanhoutte et al. 2009).
Endothelial to mesenchymal transition (EndMT) and vascular remodeling in pulmonary hypertension and idiopathic pulmonary fibrosis
Published in Expert Review of Respiratory Medicine, 2020
Archana Vijay Gaikwad, Mathew Suji Eapen, Kielan D. McAlinden, Collin Chia, Josie Larby, Stephen Myers, Surajit Dey, Greg Haug, James Markos, Allan R. Glanville, Sukhwinder Singh Sohal
The pathological origins of IPF remain undetermined, and cellular origins of the disease remain an enigma. Several cells could be affected during IPF pathogenesis, including several epithelial cell types (columnar, squamous and basal cells), type 1 and type 2 pneumocytes, vascular endothelial cells, pericytes, resident fibroblast, circulating bone-marrow-derived mesenchymal cell (fibrocytes) and resident mesenchymal cells [31]. Dysfunction of epithelial cells and aberrant mesenchymal cross talk creates an imbalance between profibrotic and antifibrotic mediators which leads to chronic fibroblast proliferation. Under pathogenic conditions, both epithelial and endothelial cells undergo a transition to their mesenchymal phenotypes, and these processes are known as epithelial to mesenchymal transition (EMT) and endothelial to mesenchymal transition (EndMT) respectively [31,32] (Figure 1(a). Both processes create a profibrotic environment by accumulating collagen-producing myofibroblasts which contributes to the overall pathogenesis of fibrotic diseases [33–35]. Recently, EndMT has gained more attention due to its potential role in lung fibrosis [36] and vascular remodeling, which primarily link to PH [37]. In the current review, we will discuss the role of this phenomenon in driving vascular remodeling. Furthermore, we discuss the EndMT mechanisms and triggers, along with the possibility of targeting EndMT as a potential therapeutic strategy for IPF patients.
Pathophysiology of large vessel vasculitis and utility of interleukin-6 inhibition therapy
Published in Modern Rheumatology, 2019
Application of TCZ will change the treatments of TAK and GCA. The targets of conventional therapy have been improvement of symptoms and reduction of serum inflammatory markers. Arterial changes (Figure 1) have been recognized as damages, and advanced cases have required surgeries. However, the new target of treatments should be prevention of vascular remodeling. The following four milestones are proposed: (1) Early diagnosis: Education of residents, primary care physicians, and the society will be important. (2) Evaluation of disease activity: Accurate and convenient disease activity indices are required. Utility of imaging modalities should be improved. (3) Treat to target: A principle should be established for prevention of vascular remodeling. (4) Standardization of treatment protocols: Revision of guidelines based on application of TCZ is needed [28].