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Flaxseed and L-Arginine, and Omega-3 Fatty Acids, per se, in Treatment of Hypertension and Sickle Cell Disease
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
In a review published in the journal Alternative Medicine Review in 2005, the authors concluded that the endothelium plays a crucial role in the maintenance of vascular tone and structure via endothelium-derived NO formed in healthy vascular endothelium from the amino acid L-arginine. Endothelial dysfunction is caused by cardiovascular risk factors, metabolic diseases and systemic or local inflammation. One possible cause of endothelial dysfunction is elevated blood levels of ADMA, an L-arginine analogue that inhibits NO formation and can, therefore, impair vascular function. Supplementation with L-arginine can restore vascular function and improve the clinical symptoms of diseases associated with vascular dysfunction. (31)
Prevention of Restenosis by Gene Targeting
Published in Eric Wickstrom, Clinical Trials of Genetic Therapy with Antisense DNA and DNA Vectors, 2020
Michael J. Mann, Victor J. Dzau, Heiko E. von der Leyen
Endothelial dysfunction plays an important role in vascular proliferative disease (Ross, 1993). The correlation between endothelial function and neointimal disease was further underscored by our observations of endothelial preservation and neointimal inhibition in genetically engineered autologous vein grafts. Denudation of the endothelium during balloon angioplasty is therefore believed to contribute to the pathogenesis of restenosis. Endothelial loss results in vasomotor abnormalities and in increased adhesion of platelets and blood borne inflammatory cells. These phenomena may be partially related to the loss of nitric oxide (NO) generation by endothelial cell nitric oxide synthase (ecNOS). Endothelial cell production of NO has other important homeostatic effects on the vessel wall (Vane et al., 1990), including inhibition of VSMC proliferation and migration, and moderation of superoxide radical generation and oxidative state. We therefore hypothesized that expression of ecNOS in VSMC after balloon injury could replace this important source of NO production and ameliorate the effects of endothelial denudation on arterial remodeling after balloon injury.
Endothelial Damage
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Stefano Masi, Rosa Maria Bruno, Lorenzo Ghiadoni, Agostino Virdis, Stefano Taddei
Homogeneous literature convincingly demonstrates the presence of endothelial damage in the hypertensive patient (14,118). Early signs of this damage manifest in the form of endothelial dysfunction. An increased vascular wall breakdown of NO is identified from the earliest stages of hypertension in humans as well as in experimental animals. This is related to an increased production of ROS in the vascular wall of hypertensive patients (118). Various enzymatic and non-enzymatic sources of ROS have been described to be activated in endothelial cells, smooth muscle cells and inflammatory cells within the arterial wall of hypertensive patients, including nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cyclooxygenase, xanthine oxidase and uncoupled eNOS (134–136). Recent evidence suggests that mitochondria could also contribute to the increased levels of vascular wall ROS detected in hypertension (137). This could induce oxidative DNA damage in the mitochondria of endothelial and smooth muscle cells (138) that may affect the synthesis of components of the respiratory chain, leading to a further increase in mtROS production, ultimately initiating a vicious cycle. Interestingly, mutations in mitochondrial DNA are also associated with increased risk of hypertension (139–141), suggesting that these alterations might precede and be in the causal pathway for the disease initiation and evolution.
Generation of a novel ex-vivo model to study re-endothelialization
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Siti Sarah Azman, Muhammad Dain Yazid, Nur Azurah Abdul Ghani, Raja Zahratul Azma Raja Sabudin, Mohd Ramzisham Abdul Rahman, Nadiah Sulaiman
Endothelial dysfunction begins with an initial injury or damage to the endothelial cells, which lead to changes in the endothelial function. These changes include impaired vasodilation, increased adhesion of leukocytes and platelets, increased vascular permeability and reduced production of nitric oxide [2]. In addition, the dysfunction triggers a phenotypic switch in SMC at the media layer leading to its proliferative state. The activated SMC start to proliferate and migrated to the intimal layer leading to IH, which results in the formation of a thickened neointima layer [7,8]. This condition contributes to the narrowing of the vessel lumen, leading to stenosis. The thickened intimal layer and altered vessel architecture due to IH can exacerbate endothelial dysfunction and perpetuate the cycle of vascular injury, inflammation and proliferation [9]. If the condition persists, it can lead to the development of several cardiovascular pathologies such as atherosclerosis, hypertension or vessel restenosis [10,11].
The oft-overlooked cardiovascular complications of inflammatory bowel disease
Published in Expert Review of Clinical Immunology, 2023
Sara Massironi, Giacomo Mulinacci, Camilla Gallo, Chiara Viganò, Maria Fichera, Andrea Villatore, Giovanni Peretto, Silvio Danese
Endothelial dysfunction, one of the earliest and most critical steps in atherosclerosis, is characterized by an impaired balance of vasodilation and vasoconstriction stimuli (mostly due to nitric oxide changes), inhibition and stimulation of smooth muscle cell proliferation and migration, and impaired thrombogenesis and fibrinolysis [40]. Microvascular endothelial dysfunction can be assessed by a number of noninvasive in vivo tests. A recent meta-analysis including 41 studies showed that IBD is associated with significant endothelial dysfunction with impaired flow-mediated dilation, one of the most commonly used noninvasive tests to assess endothelial microvasculature [41]. Similar results have been obtained in other chronic rheumatologic diseases associated with increased CVD risk, such as rheumatoid arthritis [42]. Despite scientific efforts, current guidelines do not recommend routine assessment of endothelial function to estimate cardiovascular risk in clinical practice because of limited reproducibility, difficulty in standardization, high cost, and incomplete knowledge of the pathophysiological basis [43].
Endothelial dysfunction: a therapeutic target in bacterial sepsis?
Published in Expert Opinion on Therapeutic Targets, 2021
Jean-Louis Vincent, Can Ince, Peter Pickkers
In conclusion, there is a huge potential for the prevention and/or restoration of endothelial function to improve organ function and outcomes in patients with sepsis. It is unlikely that a single molecule will be identified as a magic bullet for endothelial dysfunction in all patients. It is more likely that a subgroup of patients may benefit and that a combination of several compounds will be needed to ensure protection and facilitate restoration of endothelial function. There are many pathways and factors involved in endothelial dysfunction and many potential therapeutic strategies have already been identified. However, the lack of techniques to provide theragnostic feedback and the need to rely instead on ineffective surrogates of endothelial (dys)function has resulted in ineffective measures of therapeutic efficacy. Many questions therefore remain including which agents or combinations of agents may be effective in which patients and how this effect should best be monitored.