Relevant bibliographies by topics / PATHOLOGICAL VASCULAR REMODELING

Academic literature on the topic 'PATHOLOGICAL VASCULAR REMODELING'

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Published: 10 March 2023

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Journal articles on the topic "PATHOLOGICAL VASCULAR REMODELING"

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Ali, Zaheer, Anthony Mukwaya, Antje Biesemeier, Maria Ntzouni, Daniel Ramsköld, Sarantis Giatrellis, Parviz Mammadzada, et al. "Intussusceptive Vascular Remodeling Precedes Pathological Neovascularization." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 7 (July 2019): 1402–18. http://dx.doi.org/10.1161/atvbaha.118.312190.

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Uemura, Y., R. Shibata, K. Ohashi, T. Enomoto, Y. Kataoka, M. Miyabe, D. Yuasa, K. Matsuo, N. Ouchi, and T. Murohara. "An adipokine omentin prevents pathological vascular remodeling." European Heart Journal 34, suppl 1 (August 2, 2013): P597. http://dx.doi.org/10.1093/eurheartj/eht307.p597.

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Han, Yue, Kai Huang, Qing-Ping Yao, and Zong-Lai Jiang. "Mechanobiology in vascular remodeling." National Science Review 5, no. 6 (December 26, 2017): 933–46. http://dx.doi.org/10.1093/nsr/nwx153.

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Abstract Vascular remodeling is a common pathological process in cardiovascular diseases and includes changes in cell proliferation, apoptosis and differentiation as well as vascular homeostasis. Mechanical stresses, such as shear stress and cyclic stretch, play an important role in vascular remodeling. Vascular cells can sense the mechanical factors through cell membrane proteins, cytoskeletons and nuclear envelope proteins to initiate mechanotransduction, which involves intercellular signaling, gene expression, and protein expression to result in functional regulations. Non-coding RNAs, including microRNAs and long non-coding RNAs, are involved in the regulation of vascular remodeling processes. Mechanotransduction triggers a cascade reaction process through a complicated signaling network in cells. High-throughput technologies in combination with functional studies targeting some key hubs and bridging nodes of the network can enable the prioritization of potential targets for subsequent investigations of clinical translation. Vascular mechanobiology, as a new frontier field of biomechanics, searches for principles of stress-growth in vasculature to elucidate how mechanical factors induce biological effects that lead to vascular remodeling, with the goal of understanding the mechanical basis of the pathological mechanism of cardiovascular diseases at the cellular and molecular levels. Vascular mechanobiology will play a unique role in solving the key scientific problems of human physiology and disease, as well as generating important theoretical and clinical results.
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Wang, Zheng, Xiao Wu, Jiali Li, Qiru Guo, Zhong Jin, Hongfei Li, Bing Liang, et al. "Potassium Dehydroandrograpolide Succinate Targets NRP1 Mediated VEGFR2/VE-Cadherin Signaling Pathway to Promote Endothelial Barrier Repair." International Journal of Molecular Sciences 24, no. 4 (February 4, 2023): 3096. http://dx.doi.org/10.3390/ijms24043096.

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Impairment of vascular endothelial integrity is associated with various vascular diseases. Our previous studies demonstrated that andrographolide is critical to maintaining gastric vascular homeostasis, as well as to regulating pathological vascular remodeling. Potassium dehydroandrograpolide succinate (PDA), a derivative of andrographolide, has been clinically used for the therapeutic treatment of inflammatory diseases. This study aimed to determine whether PDA promotes endothelial barrier repair in pathological vascular remodeling. Partial ligation of the carotid artery in ApoE-/- mice was used to evaluate whether PDA can regulate pathological vascular remodeling. A flow cytometry assay, BRDU incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay and Matrigel-based tube formation assay were performed to determine whether PDA can regulate the proliferation and motility of HUVEC. A molecular docking simulation and CO-immunoprecipitation assay were performed to observe protein interactions. We observed that PDA induced pathological vascular remodeling characterized by enhanced neointima formation. PDA treatment significantly enhanced the proliferation and migration of vascular endothelial cells. Investigating the potential mechanisms and signaling pathways, we observed that PDA induced endothelial NRP1 expression and activated the VEGF signaling pathway. Knockdown of NRP1 using siRNA transfection attenuated PDA-induced VEGFR2 expression. The interaction between NRP1 and VEGFR2 caused VE-Cad-dependent endothelial barrier impairment, which was characterized by enhanced vascular inflammation. Our study demonstrated that PDA plays a critical role in promoting endothelial barrier repair in pathological vascular remodeling.
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Jia, Zhuangzhuang, Shuai Wang, Haifeng Yan, Yawen Cao, Xuan Zhang, Lin Wang, Zeyu Zhang, Shanshan Lin, Xianliang Wang, and Jingyuan Mao. "Pulmonary Vascular Remodeling in Pulmonary Hypertension." Journal of Personalized Medicine 13, no. 2 (February 19, 2023): 366. http://dx.doi.org/10.3390/jpm13020366.

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Pulmonary vascular remodeling is the critical structural alteration and pathological feature in pulmonary hypertension (PH) and involves changes in the intima, media and adventitia. Pulmonary vascular remodeling consists of the proliferation and phenotypic transformation of pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs) of the middle membranous pulmonary artery, as well as complex interactions involving external layer pulmonary artery fibroblasts (PAFs) and extracellular matrix (ECM). Inflammatory mechanisms, apoptosis and other factors in the vascular wall are influenced by different mechanisms that likely act in concert to drive disease progression. This article reviews these pathological changes and highlights some pathogenetic mechanisms involved in the remodeling process.
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Chan, Stefan, and Chen Yan. "PDE1 isozymes, key regulators of pathological vascular remodeling." Current Opinion in Pharmacology 11, no. 6 (December 2011): 720–24. http://dx.doi.org/10.1016/j.coph.2011.09.002.

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Esteban, Vanesa, Nerea Méndez-Barbero, Luis Jesús Jiménez-Borreguero, Mercè Roqué, Laura Novensá, Ana Belén García-Redondo, Mercedes Salaices, et al. "Regulator of calcineurin 1 mediates pathological vascular wall remodeling." Journal of Experimental Medicine 208, no. 10 (September 19, 2011): 2125–39. http://dx.doi.org/10.1084/jem.20110503.

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Artery wall remodeling, a major feature of diseases such as hypertension, restenosis, atherosclerosis, and aneurysm, involves changes in the tunica media mass that reduce or increase the vessel lumen. The identification of molecules involved in vessel remodeling could aid the development of improved treatments for these pathologies. Angiotensin II (AngII) is a key effector of aortic wall remodeling that contributes to aneurysm formation and restenosis through incompletely defined signaling pathways. We show that AngII induces vascular smooth muscle cell (VSMC) migration and vessel remodeling in mouse models of restenosis and aneurysm. These effects were prevented by pharmacological inhibition of calcineurin (CN) or lentiviral delivery of CN-inhibitory peptides. Whole-genome analysis revealed >1,500 AngII-regulated genes in VSMCs, with just 11 of them requiring CN activation. Of these, the most sensitive to CN activation was regulator of CN 1 (Rcan1). Rcan1 was strongly activated by AngII in vitro and in vivo and was required for AngII-induced VSMC migration. Remarkably, Rcan1−/− mice were resistant to AngII-induced aneurysm and restenosis. Our results indicate that aneurysm formation and restenosis share mechanistic elements and identify Rcan1 as a potential therapeutic target for prevention of aneurysm and restenosis progression.
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Esteban, Vanesa, Nerea Méndez-Barbero, Luis Jesús Jiménez-Borreguero, Mercè Roqué, Laura Novensá, Ana Belén García-Redondo, Mercedes Salaices, et al. "Regulator of calcineurin 1 mediates pathological vascular wall remodeling." Journal of Cell Biology 195, no. 1 (October 3, 2011): i1. http://dx.doi.org/10.1083/jcb1951oia11.

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Hong, Xuechong, and Wenduo Gu. "Plasticity of vascular resident mesenchymal stromal cells during vascular remodeling." Vascular Biology 1, no. 1 (August 12, 2019): H67—H73. http://dx.doi.org/10.1530/vb-19-0022.

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Vascular remodeling is a complex and dynamic pathological process engaging many different cell types that reside within the vasculature. Mesenchymal stromal/stem cells (MSCs) refer to a heterogeneous cell population with the plasticity to differentiate toward multiple mesodermal lineages. Various types of MSC have been identified within the vascular wall that actively contribute to the vascular remodeling process such as atherosclerosis. With the advances of genetic mouse models, recent findings demonstrated the crucial roles of MSCs in the progression of vascular diseases. This review aims to provide an overview on the current knowledge of the characteristics and behavior of vascular resident MSCs under quiescence and remodeling conditions, which may lead to the development of novel therapeutic approaches for cardiovascular diseases.
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Jin, Xin, Guo-xiang Fu, Xiao-dong Li, Ding-liang Zhu, and Ping-jin Gao. "Expression and Function of Osteopontin in Vascular Adventitial Fibroblasts and Pathological Vascular Remodeling." PLoS ONE 6, no. 9 (September 19, 2011): e23558. http://dx.doi.org/10.1371/journal.pone.0023558.

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Dissertations / Theses on the topic "PATHOLOGICAL VASCULAR REMODELING"

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Hendel, Alon. "Granzyme B in vascular remodeling and pathological angiogenesis." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44782.

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Granzyme B (GZMB) is a serine protease that is expressed by a variety of immune cells and is abundant in a large number of chronic inflammatory disorders. GZMB is highly expressed in cytotoxic lymphocytes where it serves as the main effector molecule of the granule exocytosis pathway by which cytotoxic immune cells mediate target cell death through intracellular delivery of GZMB, leading to activation of apoptotic signaling cascades. GZMB can also accumulate extracellularly during inflammation, where it can cleave a range of extracellular matrix (ECM) proteins that may disrupt cell-matrix interactions and modulate the bioavailability of matrix-bound growth factors. In this dissertation I have explored the intracellular and extracellular roles of GZMB in vascular remodeling in disease. By examining human atherosclerotic plaques, I discovered an imbalance between GZMB and its endogenous inhibitor, proteinase inhibitor 9 (PI-9). PI-9 expression by vascular smooth muscle cells (VSMC) in plaques was reduced with increased disease severity. Elevated levels of GZMB in advanced lesions were correlated with reduced PI-9 expression and increased VSMC apoptosis. These findings suggest that VSMC are more susceptible to GZMB-induced apoptosis in advanced lesions due to reduced PI-9 expression. While examining the extracellular activities of GZMB on vascular remodeling, I focused on the role of GZMB-mediated cleavage of fibronectin (FN), a known GZMB substrate. FN has a major role in regulating angiogenesis as it facilitates endothelial cell (EC) migration and capillary formation, as well as binding to angiogenic growth factors in the ECM including vascular endothelial growth factor (VEGF). VEGF is a potent vascular permeabilizing agent that is sequestered in the ECM by binding FN. GZMB-mediated FN cleavage resulted in reduced EC adhesion, migration and capillary tube formation. In addition, GZMB-mediated FN cleavage induced the release of VEGF from the ECM and promoted VEGF-dependent vascular leakage in vivo. Thus, GZMB may contribute to the progression and/or persistence of chronic inflammation by dysregulating angiogenesis and promoting vascular permeability. Collectively, the results of this work suggest that both intracellular and extracellular GZMB activities contribute to vascular remodeling and pathological angiogenesis.
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Minami, Takeya. "Reciprocal expression of MRTF-A and myocardin is crucial for pathological vascular remodeling in mice." Kyoto University, 2013. http://hdl.handle.net/2433/174774.

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Keuylian, Zela Talar. "The implication of adenylyl cyclase isoform 8 and its regulation by the Notch pathway in vascular smooth muscle cell transdifferentiation and pathological vesel remodeling." Paris 6, 2013. http://www.theses.fr/2013PA066110.

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L’athérosclérose se caractérise par le rétrécissement de la taille de la lumière des vaisseaux artériels, appelé “sténose”, par la formation de plaques d’athérome dans la paroi des artères. L’un des facteurs majeurs qui contribue à la progression de la formation des lésions est le changement phénotypique des cellules musculaires lisses médiales. Ce processus permet leur transition d’un phénotype quiescent/contractile à un phénotype sécrétoire, prolifératif et migratoire. Mes travaux consistaient à élucider une partie des mécanismes qui régule ce changement. Nous avons montré que l’expression d’une isoforme de l’enzyme adenylyl cyclase (AC), l’AC8, est impliquée dans l’inflammation et la migration des cellules musculaires lisses vasculaires. Chez l’homme, nous avons montré que les plaques d’athérosclérose expriment fortement l’AC8, principalement dans les cellules musculaires lisses de l’intima. L’AC8 était peu présent dans la média, que ce soit dans les artères pathologiques ou saines. Chez le rat, dans le modèle de resténose, nous avons montré une expression transitoire de l’AC8 régulée par la voie Notch ; in vitro, nous avons démontré que l’inhibition de la voie Notch a potentialisé l’effet de l’IL1β sur l’expression de l’AC8 et a inhibé l’expression des gènes cibles de Notch, Hrt1 et Hrt3. Dans le même modèle de resténose, l’expression transitoire de l’AC8 a coïncidé avec l’inhibition de Notch3. Ces expériences ont démontré que la voie Notch inhibe l’expression de l’AC8 induit par IL1β, et suggèrent que l’expression de l’AC8, en plus d’avoir été induite par la cytokine IL1β, dépend de l’inhibition de la voie Notch dans un contexte inflammatoire
Atherosclerosis is characterized by the narrowing of the arterial lumen termed “stenosis”, due to the expansion of arterial plaques. One of the major contributing factors to the formation of lesions and the neo-intima during post-angioplasty restenosis is the phenotypic change of medial vascular smooth muscle cells. This process switches them from a quiescent/contractile phenotype to a secretory, proliferative, migratory one. My work consisted of elucidating some of the molecular mechanisms implicated in this switch. We showed that the expression of an adenylyl cyclase (AC) isoform, AC8, is implicated in both the inflammatory and migratory properties acquired by trans-differentiated VSMCs. In human atherosclerotic arteries we showed that only intimal VSMCs strongly express AC8; very few AC8 positive VSMCs were detected in the medial layer, either in atherosclerotic or healthy arteries. In the rat balloon injury model of restenosis, we showed a transitory increase of AC8 expression. In vitro, we demonstrated that AC8 expression is regulated by the Notch pathway; inhibiting Notch amplified AC8 expression and decreased Notch target genes Hrt1 and Hrt3. In the same model of restenosis, the transitory up-regulation of AC8 expression coincided with Notch3 down-regulation. These set of experiments demonstrated that the Notch pathway decreases IL1β-mediated AC8 up-regulation in trans-differentiated VSMCs and suggests that AC8 expression, besides being induced by the proinflammatory cytokine IL1β,also depends on the down-regulation of the Notch pathway occurring in an inflammatory context. As a whole, my studies attribute a new role for AC8 in pathological vascular remodeling
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Hsieh, Nan-Kuang, and 謝楠光. "Vascular Pathological Changs and Remodeling In Various Segments of Cerebral Arteries Following Chronic Nitric Oxide Blockade: A Comparison Between Hypertensive and Normotensive Rats." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/38443779512911708563.

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博士
國防醫學院
醫學科學研究所
92
Stroke and coronary arterial disease are two major cardiovas-cular events in hypertensive patients. Cerebrovascular diseases and stroke remain the main causes of mortality and morbidity in elderly hypertensive patients. Eedogenous nitric oxide (NO) exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO production is associated with a number of cardiovascular diseases. In a series of studies, we carried out the analysis of blood pressure and vascular structure in spontaneously hypertensive rats（SHR）and normotensive Wistar-Kyoto strain（WKY）following chronic blockade of nitric oxide synthase (NOS) with Nω-nitro- L-arginine methyl ester (L-NAME). The aim of these studies were to evaluate the vascular remodelling of cerebral arteries following L-NAME in SHR and WKY.Five-wk-old male WKY and SHR were given with L-NAME (1 mg/ml) from 5th to 7th or 9th wk. The vascular remodelling and arteriolar injury score (AIS) in cerebral artery beds were assessed by various staining techniques. In WKY and SHR, L-NAME caused time-dependent elevations in tail cuff pressure (TCP) which represents the systolic arterial pressure. In SHR, L-NAME decreased body weight, but increased heart weight. The magnitude of TCP increase was much larger in SHR than WKY(＋81.0±3.2 mmHg vs.＋30.0±2.2 mmHg; p<0.01). The lumen diameter and media area of internal carotid artery (ICA) in hypertensive rats were smaller than those in untreated-WKY. These findings indicate that cerebral vascular remodelling occurs following chronic hyper- tension resulted from either genetic origin or NO deprivation. L-NAME significantly increased the media thickness in SHR, but not in WKY. Arteriolar hyalinosis and AIS in various segments of CA were assessed with periodic acid-Schiff staining and inflammatory cells were immuno- stained with the antibody against macrophage/monocyte marker (ED1). This agent also caused increase in cell volume density, AIS, inflammatory cells infiltration in perivascular space and negative growth index in ICA. The media/lumen ratio was higher in SHR than WKY, and further increased following L-NAME treatment. Diversified vascular remodelling occurred in hypertensive rats, but not in untreat-ed-WKY. These results suggest that NO deprivation and genetic hypertension cause morphological changes in various segments of cerebral arteries. ED1 positive (ED1+)cells appeared in the middle cerebral arteries of L- NAME-SHR as early as 2 wks after treatment. These cells were not observed in L-NAME-WKY and untreated-SHR. More ED1+ cells were found in L-NAME-SHR than L-NAME-WKY after 4-wk. AIS and the number of ED1+ cells around perivascular area of internal carotid artery were significantly higher in L-NAME treated rats (AIS: 137±28 in L-NAME-WKY vs 46±10 in Untreated-WKY, 169±18 in L-NAME-SHR vs 53±6 in untreated-SHR; p<0.01. ED1+ cells: 7.9 ±0.6 in L-NAME-WKY vs 1.3±0.9 in untreated-WKY, 13.6±2.7 in L-NAME-SHR vs 2.1±0.9 in Untreated-SHR; p<0.01), although TCP was higher in untreated-SHR than L-NAME-WKY(170±4 vs 137±4 mmHg; p<0.05). L-NAME significantly reduced blood flow. In low-flow states, accentuated pro-duction of mitogenic and fibrogenic growth factors such as platelet-derived growth factor and transforming growth factor-βprobably mediates inward remodelling by increas-ing smooth muscle cell hypertrophy and fibronectin deposition, whereas metalloproteinase induction provides reorganization of vessel structure. The mechanisms of decreased body weight may be L-NAME increases plasma renin activity and inhibited renin release. L-NAME attenuated the natriuresis, diuresis, and decreased proximal tubular resorption that normally accompany acute isotonic expansion of extracellular fluid volume. The mechanisms of increased heart weight may involve higher systolic blood pressure, plasma rennin activity and cardiac angiotensin converting enzyme activity in L-NAME rats than those of the subgroup without treatment of L-NAME. The hemo- dynamic load imposed on the heart is due not only to the level of blood pressure but also to concomitant hemodynamic volume load, arterial stiffness, and other factors. The hypothesis of mechanism of cardiac and vascular changes following the treatment with L-NAME might be cellular hyper- trophy due to increase inflammatory cells and proteins and apoptosis and body weight decreased due to the volume of extra- cellular fluid and interstitial components. Our study has two major findings: One is vascular cellular hypertrophy with Medial hypotrophy in L-NAME rats, besides medial thickness and cellular hypertrophy. The other is inflammatory cells expression in adventitial layer of vessels in L-NAME rats, not in subendothelial layer and untreaed-SHR. These findings suggest that ED1+ cells appeared in the middle cerebral arteries of L-NAME-SHR as early as 2 wks after treatment. Chronic inhibition of NO accelerates hypertension and induces perivascular inflammation. These important results may provide information to the mechanisms and risk factors leading to stroke.
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PACCOSI, SARA. "CARATTERIZZAZIONE DI CELLULE DENDRITICHE UMANE NEL RIMODELLAMENTO VASCOLARE PATOLOGICO PER L'INDIVIDUAZIONE DI BERSAGLI FARMACOLOGICI." Doctoral thesis, 2013. http://hdl.handle.net/2158/796857.

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Maio, Twofoot Maria Tina. "CLINICAL AND EXPERIMENTAL EVIDENCE FOR THE PATHOLOGICAL MECHANISMS UNDERLYING ASPECTS OF SEXUAL DYSFUNCTION: IMPACT OF ADIPOSITY AND CHRONIC KIDNEY DISEASE." Thesis, 2013. http://hdl.handle.net/1974/8366.

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Cardiovascular disease (CVD) and erectile dysfunction (ED) have common etiologies, such as increased adiposity and chronic diseases. Incident ED is known to be a sentinel of CVD, providing a unique opportunity for early lifestyle interventions to attenuate the progression of disease. The internal pudendal artery (IPA) plays an important role in controlling resistance to penile blood flow and thereby erections. Although morphological and functional disturbances in the IPA have been associated with ED, few studies have characterized changes in the IPA as it relates to increased adiposity and chronic diseases (e.g., chronic kidney disease [CKD]). Finally, although both vascular calcification and ED have been shown to be prevalent in patients with CKD, there has yet to be an assessment of associated mechanisms. The effect of lifestyle modifications on erectile function was evaluated in both experimental and clinical settings. Specifically, the studies assessed the effect of caloric restriction (CR) in rats and of chronic exercise in sedentary, overweight or obese male and female subjects. In rats, structural and functional changes of the IPA and erectile responses were characterized in relation to increasing adiposity and to CKD. Experimentally, the susceptibility of various vascular beds to calcification in CKD was determined. Clinically, erectile and female sexual function was assessed in patients with Stage 3 to 5 CKD, who had no history of CVD. In rats, CR blunted the accumulation of abdominal adiposity, and attenuated progression of both endothelial dysfunction and ED, independently of morphological changes in the IPA. Rats with CKD had an increased frequency of ED, greater endothelial dysfunction, and altered vascular morphology, yet vascular calcification per se did not account for ED. In the clinical study, sedentary and overweight or obese males with ED, but not females, had a significantly higher body mass index (BMI) and waist circumference. Chronic exercise significantly improved ED and female sexual dysfunction (FSD). Clinically, CKD was associated with ED and FSD as well as increased coronary artery calcification and endothelial dysfunction. These findings support the concept that early detection of cardiovascular abnormalities, using incident ED as a sentinel, should facilitate early interventions in otherwise asymptomatic populations.
Thesis (Ph.D, Pharmacology & Toxicology) -- Queen's University, 2013-09-30 22:33:20.436
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Books on the topic "PATHOLOGICAL VASCULAR REMODELING"

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1945-, Hori M., Janicki Joseph S, and Maruyama Yukio 1941-, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.

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Hori, Masatsugu, Yukio Maruyama, and Joseph S. Janicki. Cardiac-Vascular Remodeling and Functional Interaction. Springer London, Limited, 2013.

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Maruyama, Yukio. Cardiac-Vascular Remodeling and Functional Interaction. Springer, 2013.

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Hori, Masatsugu, Yukio Maruyama, and Joseph S. Janicki. Cardiac-Vascular Remodeling and Functional Interaction. Springer, 2014.

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Yang, Zhihong, and Xiu-Fen Ming. Adventitia and perivascular adipose tissue—the integral unit in vascular disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0020.

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Obesity and obesity-associated metabolic disorders are highly associated with cardiovascular disease. Abnormal ectopic deposition and accumulation of adipose tissue in organs, including perivascular space (perivascular adipose tissue, PVAT) in obesity are emerging to contribute to vascular disease development through pathological paracrine and/or endocrine secretion of cytokines, namely adipokines, which are vasoactive factors including vascular relaxing and contracting factors, smooth muscle growth promoting and inhibiting factors, and pro- and anti-inflammatory factors. In obesity, production of these factors from PVAT is altered and in imbalance which favours vascular contraction, pathological remodelling, and inflammation. In cross-talk with the endothelium, the functional changes of adventitia and PVAT are detrimental and importantly contribute to the acceleration of vascular atherosclerosis and complications associated with obesity and metabolic disorders
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Book chapters on the topic "PATHOLOGICAL VASCULAR REMODELING"

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Kawashima, Seinosuke, Ken-ichi Hirata, and Mitsuhiro Yokoyama. "Nitric Oxide and the Heart: Implications in Physiological and Pathological Conditions." In Cardiac-Vascular Remodeling and Functional Interaction, 367–79. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67041-4_28.

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Cui, Jiaxin, Mariluz Rojo Domingo, Ryan Konno, Claudia A. Manetti, George Kagugube, Oscar Odeigah, and Joakim Sundnes. "Impact of Pathological Vascular Remodelling on Right Ventricular Mechanics." In Computational Physiology, 91–109. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_7.

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AbstractPulmonary arterial hypertension (PAH) is a rare disorder characterized by elevated blood pressure and pulmonary vascular resistance, often followed by right ventricular hypertrophy and heart failure. The effect of PAH and its treatments on the mechanics, function, and remodelling of the right ventricle (RV) is currently not well understood. To study cardiac biomechanics and functionality as PAH progresses, we implemented a computational model of the heart simulating right ventricular maladaptive remodelling. Our Windkessel-based model, which accounts for direct ventricular interaction and the presence of the pericardium, is utilized to simulate various disease stages of PAH. We find that the pericardium has a larger effect on heart performance than ventricular interaction through the septum.We also examined the effectiveness of two treatments, ventricular assist device (RVAD) and atrial septostomy, on diseased hearts. We show that while both pulsatile and continuous RVADs restore cardiac function, pulsatile RVAD improves cardiac output 29.4% more than continuous RVAD. We also demonstrate that atrial septostomy improves cardiac output by 19.5%. Our model can be further extended by simulating the heart&#x2019;s response to other treatments such as extracorporeal membrane oxygenation (ECMO), and by incorporating ventricular remodelling growth simulations and finite-element ventricular modelling.
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Renna, Nicolas F., Rodrigo Garcia, Jesica Ramirez, and Roberto M. Miatello. "Vascular Repair and Remodeling: A Review." In Physiologic and Pathologic Angiogenesis - Signaling Mechanisms and Targeted Therapy. InTech, 2017. http://dx.doi.org/10.5772/67485.

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Robinson, Chapman. "Pulmonary hypertension (PHT)." In Oxford Handbook of Respiratory Medicine, edited by Stephen J. Chapman, Grace V. Robinson, Rahul Shrimanker, Chris D. Turnbull, and John M. Wrightson, 449–66. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198837114.003.0038.

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PHT is a haemodynamic and pathophysiological state that can be found in multiple clinical conditions. Each group has differing characteristic pathological features, but vasoconstriction, remodelling of the pulmonary vessel wall, medial hypertrophy of distal pulmonary arteries ± fibrotic change, and thrombosis lead to raised pulmonary vascular resistance and ultimately right heart failure. The symptoms of PHT are primarily due to RV dysfunction. The symptoms are non-specific, often leading to a delay in diagnosis from first symptoms, which include exertional breathlessness, due to the inability to increase cardiac output with exercise. WHO functional assessment classification is used to quantify the condition. Other symptoms include chest pain (right heart angina), fatigue and weakness, syncope or pre-syncope, due to a fall in systemic BP on exercise, palpitations, peripheral oedema and other signs of right-sided fluid overload.
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Conference papers on the topic "PATHOLOGICAL VASCULAR REMODELING"

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Song Hu. "Multi-parametric photoacoustic microscopy of pathological remodeling in vascular anatomy and function." In 2015 IEEE Photonics Conference (IPC). IEEE, 2015. http://dx.doi.org/10.1109/ipcon.2015.7323619.

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McGah, Patrick M., Alberto Aliseda, Daniel F. Leotta, and Kirk W. Beach. "Effects of Wall Distensibility on the Numerical Simulation of Arteriovenous Fistulae." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14183.

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Arteriovenous fistulae are created surgically to provide an adequate access for dialysis in patients with End-Stage Renal Disease (ESRD). Producing an autogenous shunt linking an artery and a vein in the peripheral circulation bypasses the high resistance capillary bed in order to provide the necessary flow rates at sites easily accessible for dialysis. It has long been recognized that hemodynamics constitute the primary external influence on the remodeling process of anastomosed vascular tissue [1, 2]. The high flow rate, together with the exposure of the venous tissue to the high arterial pressure, leads to a rapid process of wall remodeling that may lead to a mature access or end in failure. Recent hemodynamic simulations [3, 4] have computed very high viscous wall shear stresses within dialysis access fistulae; Stresses >15 Pa have been reported. These are much higher than what is typically considered normal or homeostatic (i.e. ≈ 1–1.5 Pa). The abnormal stresses in the fistulae have been hypothesized to cause pathological venous remodeling (i.e. intimal hyperplasia) which causes stenoses and threatens fistula patency. Given the high failure rate of dialysis access sites (up to 50% require surgical revision within one year), understanding the dynamics of blood flow within the fistula is a necessary step in understanding remodeling, and ultimately, in improving clinical outcomes.
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Sheidaei, A., S. C. Hunley, L. G. Raguin, and S. Baek. "Simulation of Aneurysm Growth With Stepwise Updating of Hemodynamic Loads Using an MRI-Based Geometric Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205499.

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Computer simulations of vascular tissue adaptation under various physiological and pathological conditions have emerged as a new area of research and aided researchers in their understanding of stress-mediated growth and remodeling (G&R) in these structures. With advances in computational biomechanics and biomedical imaging techniques, combinations of these advanced methods will provide promising tools for medical diagnosis and surgical planning in the future (e.g., [1]). Recently Figueroa et al. [2] presented a new computational framework that brings advances in computational biosolid and biofluid mechanics together in order to exploit new information on the biology of vascular growth and remodeling (G&R). Although the framework presented in their paper was generalized for simplicity, they did illustrate the effectiveness of this framework by applying it to a fusiform aneurysm growth with idealized geometry. In the present work, we employ this framework and test it on an anatomically realistic model of abdominal aortic aneurysm (AAA) growth. Similarly to Figueroa et al., when the stress-mediated kinetics only depends on intramural stress, the shape of the aneurysm and the expansion rate are similar to the results from the computation without using an iterative loop. However, we expect that when the stress-mediated kinetics depends on either shear or other hemodynamic components, the evolution of an AAA can change significantly.
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Baek, Seungik, C. Alberto Figueroa, Charles A. Taylor, and Jay D. Humphrey. "A Framework for Fluid-Solid-Growth Modeling and its Application to Understanding the Enlargement of a Fusiform Aneurysm." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192805.

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Blood vessels adapt in response to changes in their biomechanical and biochemical environment under various physiological and pathological conditions. While advances in computational hemodynamics and arterial wall mechanics have been spectacular, such advances have been achieved separately; there is, therefore, a pressing need for coupling biosolid and biofluid mechanics within a computationally efficient framework to study effects of fluid-solid interactions (FSI) in growth and remodeling (G&R) of the vessel wall. Toward this end, we built a fluid-solid-growth (FSG) modeling framework [1] that incorporates four separate advances by our groups: biomechanics of G&R [2], a coupled momentum method for FSI during a cardiac cycle [3], a theory of small on large for coupling G&R and FSI models [4], and improved approaches for modeling fluid boundary conditions in complex vascular systems [5]. Although the framework presented here is sufficiently general to apply to many different vascular adaptation problems, we first apply this framework to a fusiform aneurysm with a simple geometry.
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Haskett, Darren, Marie Fouts, Urs Utzinger, Doug Larson, Mohamad Azhar, and Jonathan Vande Geest. "The Effects of Angiotensin II Infusion on the Mechanical Response and Microstructural Organization of Mouse Aorta." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19635.

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Vascular diseases such as aneurysm and aortic dissection account for almost 16,000 deaths in the United States annually. In both of these diseases vascular inflammation is a common pathogenic factor. Another common pathologic feature of vascular disease includes structural matrix remodeling. It is also increasingly believed that inflammation may play a key role in the formation and progression of atherosclerotic vascular disease. Angiotensin II (AngII), a potent vasopressor, is also a strong inducer of vascular inflammation and aortic remodeling in atherosclerosis-prone mice. Based on this knowledge studies have been conducted using subcutaneous AngII infusion in order to produce aortic remodeling and aneurysm formation, with acute thoracic and abdominal aortic dissections [1].
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Graham, BB, L. Zhang, MM Mentink-Kane, H. El-Haddad, HS Champion, TA Wynn, G. Butrous, and RM Tuder. "Physiologic and Pathologic Analysis of a Murine Model of Schistosomiasis Pulmonary Vascular Remodeling." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1796.

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Coyle, K., M. Ratsep, K. Laverty, M. M. Vandenbroek, L. R. Hilton, M. Mitchell, Y. Deng, D. J. Stewart, E. Vivier, and M. L. Ormiston. "Natural Killer Cell TGFβ Signalling Influences Pulmonary Vascular Development and Pathological Vascular Remodelling in a Mouse Model of Pulmonary Arterial Hypertension." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4723.

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Liu, Fei, Margarita M. Suarez Velandia, Emeka Ifedigbo, Aleksandar Marinkovic, Xiaoli Liu, Daniel J. Tschumperlin, and Laura E. Fredenburgh. "Pathologic Matrix Stiffening Promotes Cyclooxygenase (COX)-2-Dependent Mechanobiological Feedback Amplification Of Vascular Remodeling In Pulmonary Arterial Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2622.

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