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Littérature scientifique sur le sujet « Pulmonary-arterial »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Pulmonary-arterial"

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Naik, Dr Rishabh. « Pulmonary Arterial Hypertension : Clinical and Echocardiographic Correlated Study ». Journal of Medical Science And clinical Research 05, n^o 01 (6 janvier 2017) : 15336–43. http://dx.doi.org/10.18535/jmscr/v5i1.23.

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Burt, Christiana, Joanna Pepke-Zaba et Florian Falter. « Pulmonary Arterial Hypertension ». Current Vascular Pharmacology 8, n^o 3 (1 mai 2010) : 412–20. http://dx.doi.org/10.2174/157016110791112340.

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Park, Yong Bum. « Pulmonary Arterial Hypertension ». Tuberculosis and Respiratory Diseases 67, n^o 3 (2009) : 177. http://dx.doi.org/10.4046/trd.2009.67.3.177.

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Hassoun, Paul M. « Pulmonary Arterial Hypertension ». New England Journal of Medicine 385, n^o 25 (16 décembre 2021) : 2361–76. http://dx.doi.org/10.1056/nejmra2000348.

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Goel, Khushboo, Stephanie M. Hon, Harrison W. Farber et M. Patricia George. « Pulmonary Arterial Hypertension ». Chest 160, n^o 5 (novembre 2021) : 1981–83. http://dx.doi.org/10.1016/j.chest.2021.06.010.

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O'Leary, Geraldine M. « Pulmonary arterial hypertension ». Nursing 51, n^o 11 (novembre 2021) : 37–43. http://dx.doi.org/10.1097/01.nurse.0000795272.64847.1b.

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Reingardienė, Dagmara. « Pulmonary arterial hypertension ». Medicina 43, n^o 12 (10 décembre 2007) : 978. http://dx.doi.org/10.3390/medicina43120128.

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Pulmonary arterial hypertension is a life-threatening, progressive disorder of pulmonary blood vessels leading to an increase in pressure in pulmonary artery. Diagnosis is based on a mean pulmonary artery pressure of more than 25 mmHg at rest or more than 30 mmHg during exercise. No cure exists for it yet. However, specialized treatment can lower pulmonary pressure, reduce symptoms, increase the capacity to be active, and prolong lifespan. In this review article, we attempt to summarize the current knowledge regarding clinical classification, risk factors and associated conditions, pathology and pathogenesis of this disease, diagnostic tests and detection of it, clinical course, current therapeutic strategies for the treatment of pulmonary arterial hypertension (calcium channel blockers, prostacyclin analogues, endothelin receptor antagonists, phosphodiesterase-5 inhibitors, etc.). Interventional procedures, combination therapy, and new strategies (selective serotonin reuptake inhibitors, antivascular endothelial growth factor agents, potassium channel openers, etc.) for the management of pulmonary arterial hypertension and prognosis of this rare disease are also discussed.

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Farber, Harrison W., et Joseph Loscalzo. « Pulmonary Arterial Hypertension ». New England Journal of Medicine 351, n^o 16 (14 octobre 2004) : 1655–65. http://dx.doi.org/10.1056/nejmra035488.

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McLaughlin, Vallerie V., et Michael D. McGoon. « Pulmonary Arterial Hypertension ». Circulation 114, n^o 13 (26 septembre 2006) : 1417–31. http://dx.doi.org/10.1161/circulationaha.104.503540.

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Jansa, Pavel, David Ambrož, Pavel Poláček, Jana Marešová, Michael Aschermann et Aleš Linhart. « Pulmonary arterial hypertension ». Cor et Vasa 51, n^o 7-8 (1 juillet 2009) : 455–61. http://dx.doi.org/10.33678/cor.2009.118.

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Thèses sur le sujet "Pulmonary-arterial"

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Proietti, Riccardo. « Pulmonary arterial hypertension ». Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425506.

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Strange, Julian William Nevill. « PDE5 inhibition in pulmonary arterial hypertension ». Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441986.

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Macritchie, Neil Alexander. « Modifying factors in pulmonary arterial hypertension ». Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1769/.

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Pulmonary arterial hypertension (PAH) is a debilitating disease of small pulmonary resistance arteries with vasoconstriction and vascular remodelling contributing to the disease pathology. A genetic basis for the disease was linked to heterozygous loss of function mutations in the bone morphogenetic protein receptor 2 (BMPR2) gene. The mutation is found in the majority of familial PAH cases and a significant number of apparently sporadic cases. The low penetrance of the disease in families carrying BMPR2 mutations and the absence of mutations in the majority of idiopathic patients indicates that BMPR2 deficiency alone is insufficient to induce PAH. It is generally accepted PAH has a multi-factorial pathology with endogenous and environmental factors acting in concert with genetic pre-disposition to create the disease phenotype. Enhancement of the serotonin (5-HT) system has been implicated in PAH with the 5-HT transporter (5-HTT) receiving the most attention as a modifying gene in the development of PAH and there is compelling animal and human data implicating a role for increased expression of the 5-HTT as a modulating factor. The aim of this study was to investigate if genetic pre-disposition interacts with other additional modifying factors to create the symptoms of PAH. Transgenic mice overexpressing the 5-HTT (5-HTT+), deficient in BMPR2 (BMPR2+/-) or a double transgenic (5-HTT+/BMPR2+/-) were employed in addition to mice lacking tryptophan hydroxylase 1 (Tph1), the rate limiting enzyme for the synthesis of 5-HT, and therefore lacking peripheral 5-HT (Tph1-/-). Additional known or suspected modifying factors assessed in these genetic models were hypoxia, dexfenfluramine (Dfen) and its major metabolite nordexfenfluramine (NDfen), 5-HT, bone morphogenetic protein-2 (BMP-2), KCNQ channels and the role of gender. Mice were examined in vivo for evidence of a pulmonary hypertensive phenotype following exposure to hypoxia and Dfen. Female 5-HTT+ mice were the only group tohave a rise in two indices of PAH - namely right ventricular pressure (RVP) and vascular remodelling - in room air. Female 5-HTT+ mice also had an exaggerated pulmonary hypertensive phenotype in hypoxia. BMPR2+/- mice, were, unexpectedly least susceptible to hypoxic induced increases in RVP although female mice deficient in BMPR2 (both BMPR2+/- and 5-HTT+/BMPR2+/-) had more extensive vascular remodelling under hypoxia compared with WT and 5-HTT+ mice. Male mice did not express the phenotypic changes just outlined. No synergistic effect was observed between 5-HTT+ and BMPR2+/- that resulted in a more pronounced pulmonary hypertensive phenotype. WT and BMPR2+/- mice were chronically oral-dosed with Dfen. Female mice from both genotypes developed similar degrees of PAH. Male mice did not develop elevated RVP but BMPR2+/- males did have evidence of vascular remodelling, although at a lower level than the females. Female Tph1-/- mice did not develop PAH following Dfen indicating Dfen associated PAH is dependent on peripheral 5-HT synthesis. The presence of intact 5-HT synthesis was also associated with an increased vasoconstrictor response to 5-HT in isolated intralobar pulmonary arteries (IPAs), a situation not paralleled with the other serotonergic vasoconstrictors, Dfen and NDfen, indicating differing mechanisms of action underlying the respective vasoconstrictor responses. The vasoconstrictor action of 5-HT, Dfen, NDfen and the KCNQ potassium channel blocker linopirdine were all assessed in IPAs. Pulmonary arteries from BMPR2+/- mice showed enhanced vasoconstriction to 5-HT and NDfen. 5-HTT+ and 5-HTT+/BMPR2+/- mice showed enhanced vasoconstriction to NDfen but decreased vasoconstriction to 5-HT. Female 5-HTT+/BMPR2+/- mice were the only group tested to show significantly greater vasoconstriction to Dfen compared with WT. The vasoconstrictor response to linopirdine was significantly reduced in BMPR2+/- mice but neither linopirdine nor BMP-2 affected 5- HT induced vasoconstriction. Female gender is an established risk factor for PAH. To investigate possible events that may underlie this risk, male (testosterone) and female (estradiol and 2-methoxyestradiol (2-ME)) sex hormones were assessed for their vasoactive properties in IPAs. All three hormones relaxed pre-constricted vessels but only at supraphysiological (>0.1 µM) concentrations. Each hormone also reduced the vasoconstriction exerted by 5-HT at 10-5 M in male mice but not in females. No such effect, however, was observed in either gender at a physiological (10-9 M) concentration. NDfen induced vasoconstriction was also unaffected by 10-9 M estradiol. Finally, male and female mouse lungs were assessed for protein expression of 5-HT and BMPR2 signalling compounds (p-Smad1/5/8, p-ERK1/2 and p-p38 MAPK). Female mouse lungs displayed higher expression of the mitogenic mediator p-ERK1/2 than male mouse lungs with the other proteins unchanged. In conclusion, this study confirms overexpression of the 5-HTT as a trigger for elevated RVP and vascular remodelling in mice and a cause of more severe hypoxic PAH. BMPR2+/- mice are phenotypically normal in room air and show divergent pulmonary effects following hypoxia with loss of BMPR2 seemingly attenuating hypoxic induced increases in RVP but causing a simultaneous worsening of vascular remodelling, this latter effect consistent with the important role BMPR2 has in maintaining vascular integrity. Dfen induced PAH in mice was found to be dependent on peripheral 5-HT synthesis with BMPR2 mutation not acting as a risk factor. Loss of BMPR2 can enhance vasoconstriction to serotonergic agonists and when combined with overexpression of the 5-HTT, leads to a dramatic increase in sensitivity to Dfen induced vasoconstriction. Evidence was also found for altered KCNQ channel function in transgenic animals. Unexpectedly, female gender emerged as the most crucial risk factor for PAH in this thesis.

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Zilmer, Johansen Anne Katrine. « Estrogen metabolism in pulmonary arterial hypertension ». Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5199/.

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Pulmonary arterial hypertension (PAH) is a devastating and progressive vasculopathy of the pulmonary arteries for which there is no cure. There is an urgent need for more effective therapies. PAH is characterised by elevated pulmonary arterial pressures and obstructive vascular lesions in the distal vasculature by excessive cellular proliferation. As a result, the right ventricle is placed under excessive strain resulting in adaptive hypertrophy which progresses to maladaptive hypertrophy and failure. PAH is more common in women than in men suggesting that estrogens may be integral to disease pathogenesis. Understanding the biological basis for this sex difference would offer a new treatment paradigm in this devastating cardiovascular disease. Here, we challenged the concept that the estrogen metabolic axis is dysregulated in PAH New insights have revealed a potential contribution of the estrogen metabolizing enzyme, cytochrome P450 1B1 (CYP1B1) in the development of PAH. 17β-estradiol (17β-E2) and estrone (E1) are metabolized by the activity of CYP1B1 to the 2-, 4- and 16-hydroxylated estrogens. Here, we defined the role of CYP1B1 in the pathogenesis of PAH. CYP1B1 expression was increased in both experimental (hypoxia and SU5416+hypoxia) and in heritable and idiopathic PAH (HPAH and IPAH, respectively). Both male and female CYP1B1 knockout mice (CYP1B1-/-) were challenged with chronic hypoxia to induce PAH as assessed by right ventricular systolic pressures (RVSP), right ventricular hypertrophy (RVH) and pulmonary vascular remodeling. CYP1B1-/- mice were protected against hypoxia-induced pulmonary hypertension (PH). CYP1B1 inhibition with the highly potent and selective inhibitor 2,3',4,5'-tetramethoxystilbene (TMS; 3 mg/kg/day by intra-peritoneal injection) attenuated the development of hypoxia-induced PH. Only moderate effects were observed with CYP1B1 inhibition in monocrotaline-induced PH, despite improving survival rates. Female mice that over-express the human serotonin transporter gene (SERT+ mice) develop a spontaneous PAH phenotype at 5 months of age which is dependent on circulating levels of 17β-E2. Here, we provide evidence that the estrogen metabolic axis is dysregulated in these mice and this may underlie their PAH phenotype. The estrogen synthesizing enzyme aromatase and CYP1B1 was increased in whole lung homogenates of female SERT+ mice compared to wild-type mice. Despite increased expression of aromatase, 17β-E2 concentrations were unchanged. CYP1B1 inhibition with TMS (1.5mg/kg/day by intra-peritoneal injection) attenuated the PAH phenotype in female SERT+ mice as assessed by RVSP and pulmonary vascular remodeling Other studies have identified that the 16-hydroxylated metabolites of estrogens (17β-E2 and E1) are the only CYP1B1 metabolites to induce cellular proliferation, with the most profound effects observed with 16α-hydroxyestrone (16α-OHE1). In mice exposed to chronic hypoxia, urinary concentrations of 16α-OHE1 were increased. Chronic dosing of 16α-OHE1 in mice (1.5mg/kg/day by intra-peritoneal injection for 28 days) resulted in the development of a PAH phenotype in female mice only. 16α-OHE1 induced cellular proliferation in human pulmonary arterial smooth muscle cells (hPASMCs) and this was inhibited by a scavenger of reactive oxygen species (ROS) and an inhibitor of extracellular regulated kinase 1/2 (ERK 1/2). 4-hydroxylation is the predominant metabolic pathway activated by CYP1B1 activity and we therefore investigated the effects of the 4-hydroxylated metabolite of 17β-E2 in vivo. 4-hydroxyestradiol (4-OHE2) had no effects on PAH parameters in mice (1.5mg/kg/day by intra-peritoneal injection for 28 days). However, serotonin-induced vasoconstriction of the intra-pulmonary arteries was dramatically reduced in arteries harvested from mice dosed with 4-OHE2. More recent studies have identified that 4-hydroxyestrone (4-OHE1) is the predominant CYP1B1 metabolite in the lungs of mice. Interestingly, despite evidence for a pathogenic function of CYP1B1 activity in vivo, 4-OHE1 inhibited cellular proliferation in hPASMCs as assessed by thymidine incorporation whilst no effects were reported on cell viability. We provide evidence for an altered estrogen metabolic axis in PAH, by in part, overexpression of the putatively pathological CYP1B1. Yet, the dynamic estrogen metabolic profile in pulmonary vascular cells remains undetermined. To address this, we developed a high fidelity HPLC method to quantitatively fate map estrogen metabolism in hPASMCs to determine the dynamic regulation of estrogen metabolism in PAH. We provide the first direct evidence that hPASMCs metabolize 17β-E2 and that estrogen metabolism is pathologically altered in PAH. Our metabolic screen revealed a prominent role for 17β-hydroxysteroid dehydrogenase enzymes in hPASMCs by rapid formation of E1 in all groups studied, increasing with time, with the highest activity in male control hPASMCs and the lowest activity in female control hPASMCs. In female control hPASMCs there was no evidence of CYP activity, whilst numerous metabolites were formed in the other groups studied. The formation of the pathogenic 16α-hydroxylated estrogens was only evident in PASMCs from both male and female PAH patients at 24 and 48 hours. Globally, this study introduces a platform to elucidate effects of PAH insults and potential therapies on the estrogen-metabolic profile in pulmonary vascular cells. Overall, we provide eminent evidence that the estrogen metabolic axis is pathologically altered in PAH and is influenced by gender. This provides a strong rationale for the application of estrogen-sensitive therapies in the management of this highly female discriminating disease.

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Harrison, Rachel Elizabeth. « The genetic basis of pulmonary arterial hypertension ». Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9530.

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Pulmonary arterial hypertension (PAH) can be idiopathic, hereditary, or develop in association with other diseases. Hereditary PAH is inherited as an autosomal dominant trait with reduced penetrance and variable age of onset. Heterozygous mutations in BMPR2, encoding a type II receptor in the TGF-β signalling pathway, underlie the majority of hereditary cases of PAH. PAH can occur as a rare complication of hereditary haemorrhagic telangiectasia (HHT), a vascular dysplasia caused by mutations in ALK-1, encoding a type I TGF-β receptor and ENG, encoding the accessory TGF-β receptor endoglin. BMP signalling plays an important role in cardiac embryogenesis and PAH is a common complication of congenital heart disease. In this thesis clinical and molecular studies have been performed upon a number of subjects, including those presenting with the combination of HHT and pulmonary hypertension, children presenting with PAH in childhood, and a cohort of adults and children presenting with congenital heart defects unselected for the presence of PAH. Novel heterozygous mutations were identified within the gene encoding ALK-1 and cell-based functional analysis was undertaken to characterise the consequences of these molecular defects. Novel single base pair substitutions in BMPR2 were identified in association with cardiac defects of the outflow tract, indicating that disrupted BMPRII signalling may play a role in the pathogenesis of congenital heart disease. Segregation analysis to determine allele-specific penetrance in a single multigenerational kindred demonstrated that penetrance was significantly higher than previous estimates with profound implications for clinical screening and management of families with hereditary PAH. Taken together, these studies provide insight into the molecular genetic basis of PAH, and identify disrupted signalling in the TGF-β cell-signalling pathway as a fundamental primary defect in the pathophysiology of this devastating disorder.

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James, Victoria Helen. « Molecular genetic investigation of pulmonary arterial hypertension ». Thesis, University of Leicester, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436594.

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Tonelli, Adriano R. « Treprostinil Iontophoresis In Idiopathic Pulmonary Arterial Hypertension ». Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1427825349.

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Assaggaf, Hamza M. « Molecular Risk Factors of Pulmonary Arterial Hypertension ». FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3554.

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The overall objective of the research presented in this dissertation was to investigate molecular risk factors of susceptibility to estrogenic chemicals, polychlorinated biphenyls (PCBs), hormone replacement therapy, and oral contraceptives and how that leads to the development of pulmonary arterial hypertension (PAH). Environmental and molecular risk factors for PAH are not clearly understood. This is a major hurdle for the development of new therapy against PAH as well as understanding individual susceptibility to this disease. Gender has been shown to impact the prevalence of PAH. Although controversial, estrogens have been implicated to be a risk factor for PAH. Thus, we hypothesize that women exposed to estrogenic chemicals are at increased risk of developing PAH when endocrine disrupting chemicals interact with unopposed estrogen to worsen pulmonary arterial disease. In support of this hypothesis, we have accomplished the following: Microarray data on PAH were collected and subsequent meta-analysis was conducted using genome-wide association and environment-wide association approaches on published studies as well as GEO and NHANES data. All PCB geometric mean concentrations found higher levels in people at risk of PAH than people not at risk of PAH. The sum of non-dioxin-like PCBs and the sum of dioxin-like PCBs were significantly higher in people at risk of PAH than people not at risk of PAH. Also, different levels of LOD (including PCBs concentration >LOD, > 50th percentile, 50th-75th percentile, and ≥75th percentile) were significantly higher in people at risk of PAH than people not at risk of PAH. We reported that females used estrogen pills and oral contraceptive were associated with risk of PAH. However, females used progestin and estrogen/progestin pills were not at risk of PAH. Molecular risk factor analysis using machine learning approaches revealed that VAMP2, LAMA5, POLR2C, VEGFB, and PRKCH genes are causal genes of PAH pathogenesis. Gene ontology and pathway analysis of PAH showed that genes involved in the apoptosis pathway, p53 pathway, Ras Pathway, T-cell activation, TGF-beta pathway, VEGF pathway, and Wnt pathway appear to be significantly associated with PAH. Documenting the exposure to estrogenic chemicals among the general U.S. population, and identifying agents and molecular risk factors associated with PAH have the potential to fill research gaps and facilitate our understanding of the complex role environmental chemicals play in producing toxicity in the lungs.

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Tolentino, Chelsea D. « Identifying Genetic Modifiers Contributing to Pulmonary Arterial Hypertension ». University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1377868964.

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Ferreira, Rita Marisa Nogueira. « Preventive and therapeutic strategies for pulmonary arterial hypertension ». Doctoral thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22467.

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Doutoramento em Bioquímica
A hipertensão arterial pulmonar (HAP) é uma doença grave, caracterizada por remodelação progressiva da vasculatura pulmonar, frequentemente culminando em insuficiência do ventrículo direito (VD) e morte prematura. Apesar do progresso que tem sido feito nos últimos anos em termos de opções de tratamento, a HAP permanece uma doença incurável, com um mau prognóstico e uma elevada taxa de mortalidade. No presente trabalho, pretendeu-se explorar o potencial de diferentes abordagens preventivas e terapêuticas na HAP experimental. Para isso, três estudos experimentais foram realizados a fim de avaliar o impacto do exercício físico (Estudos I e II) ou do fármaco terameprocol (TMP) (Estudo III) na HAP. No Estudo I mostramos que o exercício físico moderado realizado ao longo da vida induziu diferentes adaptações moleculares nos ventrículos esquerdo e direito. Especificamente, o VD de animais treinados apresentou maiores alterações mitocondriais, mostrando um aumento na expressão de MnSOD e SIRT3, sugestivo de uma melhoria da capacidade antioxidante. Para explorar o impacto do exercício físico na HAP, no Estudo II avaliou-se o seu potencial efeito preventivo na insuficiência do VD secundária a HAP, no modelo animal da monocrotalina (MCT) submetido a 4 semanas de exercício físico em tapete rolante antes do desenvolvimento da doença. Os resultados indicam que o pré-condicionamento com exercício físico preveniu a remodelação da artéria pulmonar e a disfunção, hipertrofia e fibrose do VD. A nível molecular, o exercício físico preveniu o aumento do rácio MHC-beta/alfa e modulou a via de sinalização TWEAK/NF-κB. O exercício físico também preveniu o aumento da expressão da atrogina-1 e induziu um aumento da atividade da MMP-2. Com o objetivo de desenvolver novas estratégias farmacológicas para o tratamento da HAP, no Estudo III foi utilizada uma abordagem proteómica baseada em espetrometria de massa para procurar as vias moleculares moduladas pelo TMP em culturas primárias de células musculares lisas da artéria pulmonar isoladas de ratos injetados com MCT. A análise bioinformática dos dados de proteómica destacou a "regulação do tamanho da célula" e "resposta ao stress do retículo endoplasmático", como processos biológicos sobre-expressos pelo TMP, enquanto os processos biológicos "resposta ao TGF-beta" e "transcrição do ADN" foram encontrados sub-expressos. Dos fatores de transcrição modulados pelo TMP, a sub-expressão do HMGB1 parece estar relacionada com o efeito anti-proliferativo deste fármaco. Estas alterações moleculares induzidas pelo tratamento com TMP podem ter contribuído para a redução da remodelação vascular e consequentemente atenuado a disfunção e hipertrofia do VD associadas à HAP induzida pela MCT. Em geral, os nossos resultados sugerem que o pré-condicionamento com exercício físico e o tratamento com TMP podem ter relevância clínica na HAP. A modulação de vias de sinalização associadas à inflamação parece estar relacionada com os efeitos benéficos destas estratégias preventivas e terapêuticas.
Pulmonary arterial hypertension (PAH) is a severe disease, characterized by progressive remodeling of the pulmonary vasculature, usually culminating in right ventricle (RV) failure and premature death. Despite the progress that has been made in the last few years in terms of treatment options, PAH remains an incurable disease, with a poor prognosis and a high mortality rate. In the current work, we intended to explore the potential of different preventive and therapeutic approaches in experimental PAH. To accomplish that, three experimental studies were performed in order to assess the impact of exercise training (Studies I and II) or the drug terameprocol (TMP) (Study III) in PAH. In Study I, we show that lifelong moderate exercise training induced different molecular adaptations in the left and right ventricles. Specifically, the RV of trained animals presented greater mitochondrial changes, showing an increased expression of MnSOD and SIRT3, suggestive of improved antioxidant capacity. To explore the impact of exercise training on PAH, in Study II we evaluated its potential preventive effect on RV failure secondary to PAH, in the monocrotaline (MCT) animal model submitted to a 4-week treadmill exercise training before disease development. Data indicate that exercise preconditioning prevented pulmonary artery remodeling and RV dysfunction, hypertrophy and fibrosis. At a molecular level, exercise training prevented the increase in beta/alpha-MHC ratio and modulated the TWEAK/NF-κB signaling pathway. Exercise training also prevented the increase of atrogin-1 expression and induced an increase in MMP-2 activity. Envisioning the development of novel pharmacological strategies for PAH treatment, in Study III we used a mass spectrometry-based proteomic approach to search for the molecular pathways modulated by TMP in pulmonary artery smooth muscle cell primary cultures isolated from rats injected with MCT. Bioinformatic analysis of proteome data highlighted the “regulation of cell size” and “response to endoplasmic reticulum stress” as biological processes up-regulated by TMP, while the biological processes “response to TGF-beta” and “DNA-templated transcription” were found down-regulated. From the transcription factors modulated by TMP, the down-regulation of HMGB1 seems to be related with the anti-proliferative effect of this drug. These molecular alterations induced by TMP treatment may have contributed to the reduction of the vascular remodeling and consequently attenuated RV dysfunction and hypertrophy associated to MCT-induced PAH. In overall, our results suggest that exercise preconditioning and TMP treatment can be of clinical relevance in PAH. The modulation of inflammation-related signaling pathways seems to be behind the benefits of these preventive and therapeutic strategies.

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Livres sur le sujet "Pulmonary-arterial"

1

Pulmonary arterial hypertension. Oxford : Clinical Pub., 2009.

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Barst, Robyn J., dir. Pulmonary Arterial Hypertension. Chichester, UK : John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470997390.

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Gerry, Coghlan, dir. Pulmonary arterial hypertension. Oxford : Oxford University Press, 2010.

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Peacock, A. J., et J. A. Barberà. Pulmonary arterial hypertension. Oxford : Clinical Pub., 2009.

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Bohnen, Michael S. Potassium Channelopathies in Pulmonary Arterial Hypertension. [New York, N.Y.?] : [publisher not identified], 2017.

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Baughman, Robert P., Roberto G. Carbone et Giovanni Bottino, dir. Pulmonary Arterial Hypertension and Interstitial Lung Diseases. Totowa, NJ : Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-074-8.

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Maurice, Beghetti, Barst Robyn J, Naeije Robert et Rubin Lewis J, dir. Pulmonary arterial hypertension related to congenital heart disease. München : Elsevier, Urban & Fischer, 2006.

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Robyn, Barst, dir. Pulmonary arterial hypertension : Diagnosis and evidence-based treatment. Chichester, West Sussex, England : John Wiley & Sons, 2008.

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Antel, J., M. B. Hesselink et R. T. Schermuly. Pulmonary arterial hypertension : Focusing on a future : enhancing and extending life. Amsterdam : IOS Press, 2010.

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P, Baughman Robert, Carbone Roberto G et Bottino Giovanni, dir. Pulmonary arterial hypertension and interstitial lung diseases : A clinical guide. Totowa, N.J : Humana, 2009.

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Chapitres de livres sur le sujet "Pulmonary-arterial"

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Thenappan, Thenappan, et Daniel Duprez. « Pulmonary Arterial Hypertension ». Dans Arterial Disorders, 313–32. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14556-3_22.

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Ntiloudi, Despina, et George Giannakoulas. « Pulmonary Arterial Hypertension ». Dans Heart Failure in Adult Congenital Heart Disease, 129–42. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77803-7_8.

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Blanco, Isabel, et Joan Albert Barberà. « Pulmonary Arterial Hypertension ». Dans Diagnostic Criteria in Autoimmune Diseases, 393–98. Totowa, NJ : Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_72.

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Söderberg, Stefan, et Michael Y. Henein. « Pulmonary Arterial Hypertension ». Dans Heart Failure in Clinical Practice, 153–63. London : Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-153-0_7.

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John, Julie, et Harold Palevsky. « Pulmonary Arterial Hypertension ». Dans Principles of Pulmonary Protection in Heart Surgery, 195–211. London : Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-308-4_21.

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Michelakis, Evangelos D., et Stephen L. Archer. « Pulmonary Arterial Hypertension ». Dans Cardiovascular Medicine, 2203–46. London : Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_108.

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Katsuragi, Shinji, et Tomoaki Ikeda. « Pulmonary Arterial Hypertension ». Dans Maternal and Fetal Cardiovascular Disease, 129–45. Singapore : Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-1993-7_12.

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Timens, Wim. « Pulmonary Arterial Hypertension ». Dans Molecular Pathology Library, 634–43. New York, NY : Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-72430-0_58.

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Boehm, Mario, et Ralph T. Schermuly. « Pulmonary Arterial Hypertension ». Dans Encyclopedia of Molecular Pharmacology, 1–8. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-21573-6_10057-1.

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Boehm, Mario, et Ralph T. Schermuly. « Pulmonary Arterial Hypertension ». Dans Encyclopedia of Molecular Pharmacology, 1328–36. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_10057.

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Actes de conférences sur le sujet "Pulmonary-arterial"

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Overbeek, Maria, Anton Vonk-Noordegraaf, Anco Boonstra et Nico Westerhof. « Right Ventriculo-arterial Coupling In Systemic Sclerosis-associated Pulmonary Arterial Hypertension Versus Idiopathic Pulmonary Arterial Hypertension ». Dans American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6591.

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Gairhe, Salina, Masahiko Oka et Ivan McMurtry. « Pulmonary Arterial Expression Of Sphingosine Kinases Is Markedly Increased In Pulmonary Arterial Hypertension ». Dans 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.a4752.

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Benza, Raymond L., Diane Vido, Mardi Gomberg-Maitland, Erika B. Rosenzweig, Adaani Frost, Priscilla Correa, Andrea Nowicki, christopher coffey et Hernan Grenett. « Pharmacogenomics In Pulmonary Arterial Hypertension ». Dans American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4882.

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Lua, S., H. Stubbs, A. Maclellan, M. Brewis, C. Church et M. Johnson. « Genetics in pulmonary arterial hypertension ». Dans ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1225.

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Yu, Y., S. Gong, P. Yuan, Y. L. Yang, R. Jiang, L. Wang, W. H. Wu, W. Xie et J. Liu. « Sex-Specific Residual Pulmonary Vasodilative Reserve as Predictors in Patients with Idiopathic Pulmonary Arterial Hypertension Pulmonary Arterial Hypertension ». Dans American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3662.

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Xanthouli, P., M. Koegler, N. Benjamin, L. Fischer, B. Egenlauf, C. Eichstaedt, S. Harutyunova et al. « Risk stratification and prognostic factors in pulmonary arterial Hypertension and pulmonary arterial Hypertension with comorbidities ». Dans 61. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e.V. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403344.

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Tamura, Yuichi, Ly Tu, Tsunehisa Yamamoto, Carole Phan, Raphael Thuillet, Alice Huertas, Morane Le Hiress, Elie Fadele, Marc Humbert et Christophe Guignabert. « Uric acid causes excessive pulmonary arterial smooth muscle cell proliferationviaURATv1 upregulation in pulmonary arterial hypertension ». Dans ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5102.

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Zhang, Zhuoli, Lan Gao, Yong Fan, Yanjie Hao et Wei Zhou. « Increased Cyr61 in pulmonary arterial hypertension involving in proliferation of pulmonary arterial smooth muscle cells ». Dans ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2477.

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Brittain, Evan L., Meredith E. Pugh, Lisa A. Wheeler, Quinn S. Wells, Ivan M. Robbins, James E. Loyd, Eric D. Austin et Anna Hemnes. « Heritable Pulmonary Arterial Hypertension Is Associated With Worse Survival Compared To Idiopathic Pulmonary Arterial Hypertension ». Dans 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.a3825.

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Winkler, T., P. Kohli, V. J. Kelly, E. G. Kehl, M. T. Kone, K. Hibbert, J. M. Rodriguez-Lopez et al. « Regional Pulmonary Vascular Resistance in Pulmonary Arterial Hypertension (PAH) ». Dans American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4513.

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Rapports d'organisations sur le sujet "Pulmonary-arterial"

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Kao, Peter N. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA : Defense Technical Information Center, juin 2010. http://dx.doi.org/10.21236/ada541337.

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Kao, Peter N. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA : Defense Technical Information Center, juin 2012. http://dx.doi.org/10.21236/ada568676.

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Kao, Peter N. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA : Defense Technical Information Center, juin 2013. http://dx.doi.org/10.21236/ada599248.

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Kao, Peter. Lineage Analysis in Pulmonary Arterial Hypertension. Fort Belvoir, VA : Defense Technical Information Center, juin 2011. http://dx.doi.org/10.21236/ada555153.

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Peng, Wen, JunFeng Zou, Feng Tang et DeDong Zheng. Effect of iron therapy for the patients of Pulmonary arterial hypertension : A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, juin 2021. http://dx.doi.org/10.37766/inplasy2021.6.0101.

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Hu, Yuqi, Hui Zhang, Fan Zhang, Xiaowen Sheng, Liru Huang et Ai Cui. Survival and Prognostic Factors in Patients with Connective Tissue Diseases Associated Pulmonary Arterial Hypertension : A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, août 2020. http://dx.doi.org/10.37766/inplasy2020.8.0005.

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Wideman, Jr., Robert F., Nicholas B. Anthony, Avigdor Cahaner, Alan Shlosberg, Michel Bellaiche et William B. Roush. Integrated Approach to Evaluating Inherited Predictors of Resistance to Pulmonary Hypertension Syndrome (Ascites) in Fast Growing Broiler Chickens. United States Department of Agriculture, décembre 2000. http://dx.doi.org/10.32747/2000.7575287.bard.

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Background PHS (pulmonary hypertension syndrome, ascites syndrome) is a serious cause of loss in the broiler industry, and is a prime example of an undesirable side effect of successful genetic development that may be deleteriously manifested by factors in the environment of growing broilers. Basically, continuous and pinpointed selection for rapid growth in broilers has led to higher oxygen demand and consequently to more frequent manifestation of an inherent potential cardiopulmonary incapability to sufficiently oxygenate the arterial blood. The multifaceted causes and modifiers of PHS make research into finding solutions to the syndrome a complex and multi threaded challenge. This research used several directions to better understand the development of PHS and to probe possible means of achieving a goal of monitoring and increasing resistance to the syndrome. Research Objectives (1) To evaluate the growth dynamics of individuals within breeding stocks and their correlation with individual susceptibility or resistance to PHS; (2) To compile data on diagnostic indices found in this work to be predictive for PHS, during exposure to experimental protocols known to trigger PHS; (3) To conduct detailed physiological evaluations of cardiopulmonary function in broilers; (4) To compile data on growth dynamics and other diagnostic indices in existing lines selected for susceptibility or resistance to PHS; (5) To integrate growth dynamics and other diagnostic data within appropriate statistical procedures to provide geneticists with predictive indices that characterize resistance or susceptibility to PHS. Revisions In the first year, the US team acquired the costly Peckode weigh platform / individual bird I.D. system that was to provide the continuous (several times each day), automated weighing of birds, for a comprehensive monitoring of growth dynamics. However, data generated were found to be inaccurate and irreproducible, so making its use implausible. Henceforth, weighing was manual, this highly labor intensive work precluding some of the original objectives of using such a strategy of growth dynamics in selection procedures involving thousands of birds. Major conclusions, solutions, achievements 1. Healthy broilers were found to have greater oscillations in growth velocity and acceleration than PHS susceptible birds. This proved the scientific validity of our original hypothesis that such differences occur. 2. Growth rate in the first week is higher in PHS-susceptible than in PHS-resistant chicks. Artificial neural network accurately distinguished differences between the two groups based on growth patterns in this period. 3. In the US, the unilateral pulmonary occlusion technique was used in collaboration with a major broiler breeding company to create a commercial broiler line that is highly resistant to PHS induced by fast growth and low ambient temperatures. 4. In Israel, lines were obtained by genetic selection on PHS mortality after cold exposure in a dam-line population comprising of 85 sire families. The wide range of PHS incidence per family (0-50%), high heritability (about 0.6), and the results in cold challenged progeny, suggested a highly effective and relatively easy means for selection for PHS resistance 5. The best minimally-invasive diagnostic indices for prediction of PHS resistance were found to be oximetry, hematocrit values, heart rate and electrocardiographic (ECG) lead II waves. Some differences in results were found between the US and Israeli teams, probably reflecting genetic differences in the broiler strains used in the two countries. For instance the US team found the S wave amplitude to predict PHS susceptibility well, whereas the Israeli team found the P wave amplitude to be a better valid predictor. 6. Comprehensive physiological studies further increased knowledge on the development of PHS cardiopulmonary characteristics of pre-ascitic birds, pulmonary arterial wedge pressures, hypotension/kidney response, pulmonary hemodynamic responses to vasoactive mediators were all examined in depth. Implications, scientific and agricultural Substantial progress has been made in understanding the genetic and environmental factors involved in PHS, and their interaction. The two teams each successfully developed different selection programs, by surgical means and by divergent selection under cold challenge. Monitoring of the progress and success of the programs was done be using the in-depth estimations that this research engendered on the reliability and value of non-invasive predictive parameters. These findings helped corroborate the validity of practical means to improve PHT resistance by research-based programs of selection.

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