Endothelial Dysfunction - Old Concepts and New Challenges最新文献_第2页

Endothelial Dysfunction in Type 2 Diabetes: Targeting Inflammation 2型糖尿病的内皮功能障碍:针对炎症

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2018-10-24 DOI: 10.5772/INTECHOPEN.76994

C. Sena, F. Carrilho, R. Seiça

{"title":"Endothelial Dysfunction in Type 2 Diabetes: Targeting Inflammation","authors":"C. Sena, F. Carrilho, R. Seiça","doi":"10.5772/INTECHOPEN.76994","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.76994","url":null,"abstract":"Several experimental and clinical studies have indicated a prominent role of vascular inflammation in the development of endothelial dysfunction. In endothelial dysfunction, the endothelium loses its physiological features, decrements nitric oxide bioavailability, and shifts towards a vasoconstrictor, pro-thrombotic and pro-inflammatory state. Within arterial wall, the interplay between the pro-inflammatory and pro-oxidant milieus promotes vascular dysfunction, and perivascular adipose tissue seems to play an important role. Inflammation is now considered a key event in vascular dysfunction and the development of vascular disease associated with obesity and type 2 diabetes. This concept is supported by the fact that anti-inflammatory adipokines such as adiponectin protect endothelial function, and interventions resulting in reduced inflammation such as the administration of salicylates prevent vascular dysfunction and cardiovascular events. Thus, the aim of this review is to address the role of inflammation and its mechanisms in endothelial dysfunction associated with diabetes, describing the impact of these conditions on vascular function.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"335 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124708396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Targeting Endothelial SIRT1 for the Prevention of Arterial Aging 靶向内皮细胞SIRT1预防动脉老化

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2018-02-22 DOI: 10.5772/INTECHOPEN.73019

Yumeng Guo, Yu Wang

引用次数: 3

Smoking, Respiratory Diseases and Endothelial Dysfunction 吸烟、呼吸系统疾病和内皮功能障碍

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2018-02-03 DOI: 10.5772/INTECHOPEN.73555

V. Nevzorova, T. Brodskaya, N. Zakharchuk

{"title":"Smoking, Respiratory Diseases and Endothelial Dysfunction","authors":"V. Nevzorova, T. Brodskaya, N. Zakharchuk","doi":"10.5772/INTECHOPEN.73555","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.73555","url":null,"abstract":"Vascular endothelium actively participates in inflammatory reactions in the majority of chronic respiratory diseases. Smoking is a major risk factor for bronchopulmonary diseases, and it plays an important role in endothelial dysfunction development. Some experiments prove that aggressive pollutants of tobacco smoke (benzopyrene, peroxynitrite, acrolein, cyanides, peroxides, etc.) can cause direct damage to endothelial cells due to expression of adhesion molecules on their surface and intensification of lipid peroxidation. In turn, oxi-dized lipoproteins in the tunica intima of the vessel work as attractants for chemotaxis of leukocytes and monocytes that start to produce pro-inflammatory cytokines in big amounts. These processes trigger systemic inflammatory response that leads to irreversible thickening of the vessel walls and deterioration of their mechanical properties. Chronic exposure to tobacco smoke and the products of combustion of tobacco leads to chronic system inflam- matory reaction, oxidative stress, endothelial dysfunction and morpho-functional damage of target organs. Nowadays, the connection between chronic obstructive pulmonary disease (COPD) and some cardiovascular and cerebrovascular diseases has been well established. Studying the mechanisms of endothelial dysfunction in brain blood vessels of patients with smoking habits and COPD can be very important for preventing acute vascular events.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132138487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Vascular Sympathetic Neurotransmission and Endothelial Dysfunction 血管交感神经传递与内皮功能障碍

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2017-12-27 DOI: 10.5772/INTECHOPEN.72442

J. Sousa, C. Diniz

{"title":"Vascular Sympathetic Neurotransmission and Endothelial Dysfunction","authors":"J. Sousa, C. Diniz","doi":"10.5772/INTECHOPEN.72442","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.72442","url":null,"abstract":"Endothelium is an important regulator of vascular tone via release of various endothelium- derived substances. Several studies have reported that endothelium may decrease the release of noradrenaline from vascular postganglionic sympathetic nerves and thus neuro- genic vasoconstriction. Endothelium derived-mediators (adenosine and NO) can modify vascular sympathetic neurotransmission and are relevant for vascular homeostasis. This is a relevant issue in terms of vascular homeostasis and, any modification, may lead to a deregulation process and to pathologies. Focus on NO-mediated effects on vascular sym- pathetic transmission will be done, discriminating the effects ascribed to NO generated by NO synthases located in the different vascular layers. A comparison between mesenteric/ tail arteries will also be explored, particularly the relevance of the transsynaptic modulation on noradrenaline release mediated by endothelial NO and adenosine in normotensive/ hypertensive vascular tissues. Adenosinergic system, namely adenosine, nucleoside transporters and adenosine receptors, can be influenced by endothelium mediators, namely by NO, causing alterations on the way these players interact with each other. In conditions where endothelium is compromised, a deregulation occurs with an increase in vascular sympathetic neurotransmission (as a consequence of adenosinergic system dynamic alter-ation). In summary, the impact of endothelial dysfunction on vascular neurotransmission is debated with particular focus on adenosinergic and nitroxidergic system dynamics.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"16 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126586549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Selected Endothelial Responses after Ionizing Radiation Exposure 电离辐射暴露后选择的内皮反应

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2017-12-20 DOI: 10.5772/INTECHOPEN.72386

Bjorn Baselet, Raghda Ramadan, Abderrafi MohammedBenotmane, P. Sonveaux, S. Baatout, A. Aerts

{"title":"Selected Endothelial Responses after Ionizing Radiation Exposure","authors":"Bjorn Baselet, Raghda Ramadan, Abderrafi MohammedBenotmane, P. Sonveaux, S. Baatout, A. Aerts","doi":"10.5772/INTECHOPEN.72386","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.72386","url":null,"abstract":"Along with the development of novel chemotherapeutic agents, radiation therapy has revolutionized the prognosis of patients with various cancers. However, with a longer life expectancy, radiation treatment-related comorbidity, like cardiovascular diseases (CVDs), becomes an issue for cancer survivors. In addition, exposure to X-rays for medical diagnostics is dramatically increasing at the present times. A pressing question is whether or not exposure to these very low doses can cause health damage. Below 0.5 gray (Gy), an increased risk cannot be evidenced by epidemiology alone, and in vitro and in vivo mechanistic studies focused on the elucidation of molecular signaling pathways are needed. Given the critical role of the endothelium in normal vascular functions, a complete understanding of radiation-induced endothelial dysfunction is crucial. In this way, the current radiation protection system could be refined if needed, making it possible to more accurately assess the cardiovascular risk in the low-dose region. Finally, radiation-induced CVD, like CVD in general, is a progressive disorder that may take years to decades to manifest. Therefore, experimental studies are warranted to fulfill the urgent need to identify noninvasive biomarkers for an early detection and potential interventions—together with a healthy lifestyle—that may prevent or mitigate these adverse effects.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"24 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133664180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Angiogenesis in Adipose Tissue: How can Moderate Caloric Restriction Affects Obesity-Related Endothelial Dysfunction? 脂肪组织血管生成:适度热量限制如何影响肥胖相关的内皮功能障碍?

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2017-12-20 DOI: 10.5772/INTECHOPEN.72624

K. Korybalska

{"title":"Angiogenesis in Adipose Tissue: How can Moderate Caloric Restriction Affects Obesity-Related Endothelial Dysfunction?","authors":"K. Korybalska","doi":"10.5772/INTECHOPEN.72624","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.72624","url":null,"abstract":"The plasticity of adipose tissue (AT) is related to its angiogenic ability. Angiogenesis is a multistep process which involves endothelial cell (EC) proliferation, migration, invasion and finally tube formation. AT as a secretory organ produces adipokines, which contributes to the development of subclinical inflammation. The inflammation-related adipokines deteriorate EC function and in consequence change the production of endothelial mediators responsible for vascular homeostasis and angiogenesis, leading to cardiovascular diseases (CVD) in obese patients. Additionally, the recent observation suggests that AT is poorly oxygenated in obesity. Hypoxia limits the healthy expansion of AT and stimulates a molecular response, enhancing nuclear factor kappa-B (NF-kB) and hypoxia-inducible factor (HIF-1) expression. HIF-1α induction does not start a normal angiogenic process but rather induces inflammatory response and fibrosis that is strongly associated with insulin resistance (IR). It is believed that EC dysfunction in obesity can be reduced by caloric restriction (CR). Moderate CR reflects a real-life situation and could be optimal to achieve an EC improvement. It reduces adiposity leading to pro-angiogenic, anti-inflammatory and—to a lesser extent—anti-oxidative cellular effects, which not only preserves the healthy EC phenotype but also leads to an improvement of AT remodeling and prevent systemic IR.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"104 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133855863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Hyperglycemia-Induced Endothelial Dysfunction 高血糖诱导的内皮功能障碍

Endothelial Dysfunction - Old Concepts and New Challenges Pub Date : 2017-12-20 DOI: 10.5772/INTECHOPEN.71433

Domokos Gerő

{"title":"Hyperglycemia-Induced Endothelial Dysfunction","authors":"Domokos Gerő","doi":"10.5772/INTECHOPEN.71433","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.71433","url":null,"abstract":"Glucose-induced endothelial dysfunction plays a fundamental role in the development of diabetic vascular complications and glycemic control (the foundation of diabetes care) provides limited protection against the cardiovascular complications. Therefore, iden- tification of novel drug targets and treatment approaches for diabetes complications represent a key direction of current pharmaceutical research. The “unifying theory” of hyperglycemia-induced endothelial cell injury organizes the events of cellular dysfunction in a linear cascade and identifies mitochondrial superoxide generation as the trig - gering event of the injury. Exposure to high glucose concentration for long periods or repeated glycemic swings may induce changes in metabolic substrate availability and lead to mitochondrial hyperpolarization. Changes in the mitochondrial membrane potential induce superoxide production by the electron transport chain and result in oxidative stress. Mitochondrial superoxide is also responsible for the induction of other sources of reactive oxygen species (ROS) within the cells, including advanced glycation end prod - ucts (AGEs) and the NADPH oxidase. Mitochondria also show morphological changes and impaired assembly of the respiratory complexes occurs, which results in cellular energy failure, cell senescence and vascular dysfunction. Current intervention strategies aim to inhibit the mitochondrial ROS production and novel therapeutic approaches are expected to provide valuable tools in diabetes therapy in the upcoming years.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"13 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126918235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 20