scholarly journals Potential Benefits of Flavonoids on the Progression of Atherosclerosis by Their Effect on Vascular Smooth Muscle Excitability

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3557
Author(s):  
Rosa Edith Grijalva-Guiza ◽  
Aura Matilde Jiménez-Garduño ◽  
Luis Ricardo Hernández
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Ion Channels ◽  
Vascular Smooth Muscle ◽  
Ion Channel ◽  
Redox Potential ◽  
Related Condition ◽  
Potential Benefits ◽  
Muscle Excitability ◽  
Progression Of Atherosclerosis

Flavonoids are a group of secondary metabolites derived from plant-based foods, and they offer many health benefits in different stages of several diseases. This review will focus on their effects on ion channels expressed in vascular smooth muscle during atherosclerosis. Since ion channels can be regulated by redox potential, it is expected that during the onset of oxidative stress-related diseases, ion channels present changes in their conductive activity, impacting the progression of the disease. A typical oxidative stress-related condition is atherosclerosis, which involves the dysfunction of vascular smooth muscle. We aim to present the state of the art on how redox potential affects vascular smooth muscle ion channel function and summarize if the benefits observed in this disease by using flavonoids involve restoring the ion channel activity.

scholarly journals Kv1.3 channel inhibition limits uremia-induced calcification in mouse and human vascular smooth muscle

Function ◽  
2020 ◽  
Author(s):  
Violeta Cazaña-Pérez ◽  
Pilar Cidad ◽  
Juan F Navarro-González ◽  
Jorge Rojo-Mencía ◽  
Frederic Jaisser ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Ion Channels ◽  
Vascular Smooth Muscle ◽  
Ion Channel ◽  
Mineral Metabolism ◽  
K Channel ◽  
Human Aorta ◽  
Genetic Ablation ◽  
Channel Inhibition

Abstract Chronic kidney disease (CKD) significantly increases cardiovascular risk. In advanced CKD stages, accumulation of toxic circulating metabolites and mineral metabolism alterations triggers vascular calcification, characterized by vascular smooth muscle cell (VSMC) transdifferentiation and loss of the contractile phenotype. Phenotypic modulation of VSMC occurs with significant changes in gene expression. Even though ion channels are an integral component of VSMC function, the effects of uremia on ion channel remodeling has not been explored. We used an in vitro model of uremia-induced calcification of human aorta smooth muscle cells (HASMC) to study the expression of 92 ion channel subunit genes. Uremic serum induced extensive remodeling of ion channel expression consistent with loss of excitability but different from the one previously associated to transition from contractile to proliferative phenotypes. Among the ion channels tested, we found increased abundance and activity of voltage-dependent K+ channel Kv1.3. Enhanced Kv1.3 expression was also detected in aorta from a mouse model of CKD. Pharmacological inhibition or genetic ablation of Kv1.3 decreased the amount of calcium phosphate deposition induced by uremia, supporting an important role for this channel on uremia-induced VSMC calcification.

Oxidative Stress Produced with Cell Migration Increases Synthetic Phenotype of Vascular Smooth Muscle Cells

2005 ◽  
Vol 33 (11) ◽  
pp. 1546-1554 ◽  
Author(s):  
Hak-Joon Sung ◽  
Suzanne G. Eskin ◽  
Yumiko Sakurai ◽  
Andrew Yee ◽  
Noriyuki Kataoka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Synthetic Phenotype

scholarly journals Calcific Uremic Arteriolopathy: Pathophysiology, Reactive Oxygen Species and Therapeutic Approaches

2010 ◽  
Vol 3 (2) ◽  
pp. 109-121 ◽  
Author(s):  
Kurt M. Sowers ◽  
Melvin R. Hayden
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Smooth Muscle ◽  
Kidney Disease ◽  
Vascular Smooth Muscle ◽  
Reactive Oxygen ◽  
Morbidity And Mortality ◽  
Oxygen Species ◽  
Calcific Uremic Arteriolopathy

Calcific uremic arteriolopathy (CUA)/calciphylaxis is an important cause of morbidity and mortality in patients with chronic kidney disease requiring renal replacement. Once thought to be rare, it is being increasingly recognized and reported on a global scale. The uremic milieu predisposes to multiple metabolic toxicities including increased levels of reactive oxygen species and inflammation. Increased oxidative stress and inflammation promote this arteriolopathy by adversely affecting endothelial function resulting in a prothrombotic milieu and significant remodeling effects on vascular smooth muscle cells. These arteriolar pathological effects include intimal hyperplasia, inflammation, endovascular fibrosis and vascular smooth muscle cell apoptosis and differentiation into bone forming osteoblast-like cells resulting in medial calcification. Systemic factors promoting this vascular condition include elevated calcium, parathyroid hormone and hyperphosphatemia with consequent increases in the calcium × phosphate product. The uremic milieu contributes to a marked increased in upstream reactive oxygen species—oxidative stress and subsequent downstream increased inflammation, in part, via activation of the nuclear transcription factor NFκB and associated downstream cytokine pathways. Consitutive anti-calcification proteins such as Fetuin-A and matrix GLA proteins and their signaling pathways may be decreased, which further contributes to medial vascular calcification. The resulting clinical entity is painful, debilitating and contributes to the excess morbidity and mortality associated with chronic kidney disease and end stage renal disease. These same histopathologic conditions also occur in patients without uremia and therefore, the term calcific obliterative arteriolopathy could be utilized in these conditions.

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