scholarly journals Vascular Stiffness in Aging and Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Stephen F. Vatner ◽  
Jie Zhang ◽  
Christina Vyzas ◽  
Kalee Mishra ◽  
Robert M. Graham ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Protective Role ◽  
Vascular Stiffness ◽  
Calcium Deposition ◽  
Female Sex Hormones ◽  
Age Related ◽  
Before And After ◽  
Males And Females ◽  
Human Primate

The goal of this review is to provide further understanding of increased vascular stiffness with aging, and how it contributes to the adverse effects of major human diseases. Differences in stiffness down the aortic tree are discussed, a topic requiring further research, because most prior work only examined one location in the aorta. It is also important to understand the divergent effects of increased aortic stiffness between males and females, principally due to the protective role of female sex hormones prior to menopause. Another goal is to review human and non-human primate data and contrast them with data in rodents. This is particularly important for understanding sex differences in vascular stiffness with aging as well as the changes in vascular stiffness before and after menopause in females, as this is controversial. This area of research necessitates studies in humans and non-human primates, since rodents do not go through menopause. The most important mechanism studied as a cause of age-related increases in vascular stiffness is an alteration in the vascular extracellular matrix resulting from an increase in collagen and decrease in elastin. However, there are other mechanisms mediating increased vascular stiffness, such as collagen and elastin disarray, calcium deposition, endothelial dysfunction, and the number of vascular smooth muscle cells (VSMCs). Populations with increased longevity, who live in areas called “Blue Zones,” are also discussed as they provide additional insights into mechanisms that protect against age-related increases in vascular stiffness. Such increases in vascular stiffness are important in mediating the adverse effects of major cardiovascular diseases, including atherosclerosis, hypertension and diabetes, but require further research into their mechanisms and treatment.

scholarly journals The Dual Role of Vitamin K2 in “Bone-Vascular Crosstalk”: Opposite Effects on Bone Loss and Vascular Calcification

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1222
Author(s):  
Domitilla Mandatori ◽  
Letizia Pelusi ◽  
Valeria Schiavone ◽  
Caterina Pipino ◽  
Natalia Di Pietro ◽  
...  
Keyword(s):  
Bone Loss ◽  
Vascular Calcification ◽  
Vascular System ◽  
The Elderly ◽  
Food Supplement ◽  
Vitamin K2 ◽  
Bioactive Molecules ◽  
Calcium Deposition ◽  
Age Related

Osteoporosis (OP) and vascular calcification (VC) represent relevant health problems that frequently coexist in the elderly population. Traditionally, they have been considered independent processes, and mainly age-related. However, an increasing number of studies have reported their possible direct correlation, commonly defined as “bone-vascular crosstalk”. Vitamin K2 (VitK2), a family of several natural isoforms also known as menaquinones (MK), has recently received particular attention for its role in maintaining calcium homeostasis. In particular, VitK2 deficiency seems to be responsible of the so-called “calcium paradox” phenomenon, characterized by low calcium deposition in the bone and its accumulation in the vessel wall. Since these events may have important clinical consequences, and the role of VitK2 in bone-vascular crosstalk has only partially been explained, this review focuses on its effects on the bone and vascular system by providing a more recent literature update. Overall, the findings reported here propose the VitK2 family as natural bioactive molecules that could be able to play an important role in the prevention of bone loss and vascular calcification, thus encouraging further in-depth studies to achieve its use as a dietary food supplement.

scholarly journals The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases

2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Atherosclerotic Disease ◽  
Cardiac Diseases ◽  
Compensatory Response ◽  
Age Related ◽  
Anti Oxidant ◽  
Progression Of Atherosclerosis

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.

The Protective Role of Exercise Against Age-Related Neurodegeneration

2021 ◽  
pp. 101543
Author(s):  
Alyson L. Sujkowski ◽  
Luke Hong ◽  
R.J. Wessells ◽  
Sokol V. Todi
Keyword(s):  
Protective Role ◽  
Age Related

scholarly journals Physical Activity Prevents Cartilage Degradation: A Metabolomics Study Pinpoints the Involvement of Vitamin B6

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1374 ◽  
Author(s):  
Deiana ◽  
Malerba ◽  
Dalle Carbonare ◽  
Cheri ◽  
Patuzzo ◽  
...  
Keyword(s):  
Physical Activity ◽  
Vitamin B6 ◽  
Cartilage Degradation ◽  
Protective Role ◽  
Before And After ◽  
Metabolomics Study ◽  
Cartilage Cells ◽  
First Time ◽  
Chondrosarcoma Cell Line

Osteoarthritis (OA) is predominantly characterized by the progressive degradation of articular cartilage, the connective tissue produced by chondrocytes, due to an imbalance between anabolic and catabolic processes. In addition, physical activity (PA) is recognized as an important tool for counteracting OA. To evaluate PA effects on the chondrocyte lineage, we analyzed the expression of SOX9, COL2A1, and COMP in circulating progenitor cells following a half marathon (HM) performance. Therefore, we studied in-depth the involvement of metabolites affecting chondrocyte lineage, and we compared the metabolomic profile associated with PA by analyzing runners’ sera before and after HM performance. Interestingly, this study highlighted that metabolites involved in vitamin B6 salvage, such as pyridoxal 5’-phosphate and pyridoxamine 5’-phosphate, were highly modulated. To evaluate the effects of vitamin B6 in cartilage cells, we treated differentiated mesenchymal stem cells and the SW1353 chondrosarcoma cell line with vitamin B6 in the presence of IL1β, the inflammatory cytokine involved in OA. Our study describes, for the first time, the modulation of the vitamin B6 salvage pathway following PA and suggests a protective role of PA in OA through modulation of this pathway.

scholarly journals Involvement of insulin resistance in D-galactose-induced age-related dementia in rats: Protective role of metformin and saxagliptin

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183565 ◽  
Author(s):  
Sara Kenawy ◽  
Rehab Hegazy ◽  
Azza Hassan ◽  
Siham El-Shenawy ◽  
Nawal Gomaa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protective Role ◽  
Age Related

scholarly journals Autophagy Protects Advanced Glycation End Product-Induced Apoptosis and Expression of MMP-3 and MMP-13 in Rat Chondrocytes

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Wenzhou Huang ◽  
Peng Ao ◽  
Jian Li ◽  
Tianlong Wu ◽  
Libiao Xu ◽  
...  
Keyword(s):  
Western Blotting ◽  
Annexin V ◽  
Protective Role ◽  
Autophagic Flux ◽  
Advanced Glycation ◽  
Age Related ◽  
Glycation End Products ◽  
Induced Apoptosis ◽  
Related Proteins

Aging is one of the most prominent risk factors for the pathological progression of osteoarthritis (OA). One feature of age-related changes in OA is advanced glycation end products (AGEs) accumulation in articular cartilage. Autophagy plays a cellular housekeeping role by removing dysfunctional cellular organelles and proteins. However, the relationship between autophagy and AGE-associated OA is unknown. The aim of this study is to determine whether autophagy participates in the pathology of AGE-treated chondrocytes and to investigate the exact role of autophagy in AGE-induced cell apoptosis and expression of matrix metalloproteinase- (MMP-) 3 and MMP-13. AGEs induced notable apoptosis that was detected by Annexin V/PI double-staining, and the upregulation of MMP-3 and MMP-13 was confirmed by Western blotting. Autophagy-related proteins were also determined by Western blotting, and chondrocytes were transfected with mCherry-GFP-LC3B-adenovirus to monitor autophagic flux. As a result, autophagy significantly increased in chondrocytes and peaked at 6 h. Furthermore, rapamycin (RA) attenuated AGE-induced apoptosis and expression of MMP-3 and MMP-13 by autophagy activation. In contrast, pretreatment with autophagy inhibitor 3-methyladenine (3-MA) enhanced the abovementioned effects of AGEs. We therefore demonstrated that autophagy is linked with AGE-related pathology in rat chondrocytes and plays a protective role in AGE-induced apoptosis and expression of MMP-3 and MMP-13.

scholarly journals Phytochemicals Mediated Remediation of Neurotoxicity Induced by Heavy Metals

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Vivek Kumar Gupta ◽  
Shweta Singh ◽  
Anju Agrawal ◽  
Nikhat Jamal Siddiqi ◽  
Bechan Sharma
Keyword(s):  
Heavy Metals ◽  
Free Radicals ◽  
Adverse Effects ◽  
Current Knowledge ◽  
Protective Role ◽  
Cellular Systems ◽  
Cadmium Lead ◽  
Abiotic And Biotic Factors ◽  
Almost All

Almost all the environmental components including both the abiotic and biotic factors have been consistently threatened by excessive contamination of heavy metals continuously released from various sources. Different heavy metals have been reported to generate adverse effects in many ways. Heavy metals induced neurotoxicity and impairment in signalling cascade leading to cell death (apoptosis) has been indicated by several workers. On one hand, these metals are required by the cellular systems to regulate various biological functions of normal cells, while on the other their biomagnification in the cellular systems produces adverse effects. The mechanism by which the heavy metals induce neurotoxicity follows free radicals production pathway(s) specially the generation of reactive oxygen species and reactive nitrogen species. These free radicals produced in excess have been shown to create an imbalance between the oxidative and antioxidative systems leading to emergence of oxidative stress, which may cause necrosis, DNA damage, and many neurodegenerative disorders. This mini review summarizes the current knowledge available on the protective role of varied natural products isolated from different herbs/plants in imparting protection against heavy metals (cadmium, lead, arsenic, and mercury) mediated neurotoxicity.

scholarly journals Peran Spiritual Emotional Freedom Technique dalam Penanganan Nosocomephobia

ESOTERIK ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. 282
Author(s):  
Rinova Cahyandari
Keyword(s):  
Data Collection ◽  
Adverse Effects ◽  
Anxiety Disorders ◽  
Hospital Anxiety ◽  
Risk Of Death ◽  
Before And After ◽  
Psychiatric Conditions

<p class="06IsiAbstrak">The Role of Spiritual Emotional Freedom Technique in Handling <em>Nosocomephobia</em>. This article aims to find out how the role of SEFT in dealing with psychiatric conditions, namely in cases of anxiety disorders, especially in hospital anxiety (<em>nosocomephobia</em>). <em>Nosocomephobia</em> can be defined as excessive fear associated with hospitals. Efforts to manage <em>nosocomephobia</em> become very important to do because in general patients with <em>nosocomepobia</em> will refuse to go to the hospital and as a result, adverse effects include the risk of death. The data collection in this article was obtained through the subject's statement regarding judgments related to anxiety that arises. Analysis of the data in this article is done by comparing the level of anxiety before and after therapy. The result showed a decrease in judgment related to the condition of perceived anxiety. The success of SEFT in reducing anxiety can be influenced by the existence of faith, solemnity, sincerity, resignation, and grateful to Allah Swt.</p>

scholarly journals Sex-Specific Retinal Anomalies Induced by Chronic Social Defeat Stress in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Eric Arsenault ◽  
Andrée-Anne Lavigne ◽  
Samaneh Mansouri ◽  
Anne-Marie Gagné ◽  
Kimberley Francis ◽  
...  
Keyword(s):  
Social Defeat ◽  
Oscillatory Potentials ◽  
Social Defeat Stress ◽  
Major Depressive ◽  
Retinal Activity ◽  
Age Related ◽  
Chronic Social Defeat Stress ◽  
Before And After ◽  
Males And Females ◽  
Age Related Changes

Major depressive disorder (MDD) is one of the most common consequences of chronic stress. Still, there is currently no reliable biomarker to detect individuals at risk to develop the disease. Recently, the retina emerged as an effective way to investigate psychiatric disorders using the electroretinogram (ERG). In this study, cone and rod ERGs were performed in male and female C57BL/6 mice before and after chronic social defeat stress (CSDS). Mice were then divided as susceptible or resilient to stress. Our results suggest that CSDS reduces the amplitude of both oscillatory potentials and a-waves in the rods of resilient but not susceptible males. Similar effects were revealed following the analysis of the cone b-waves, which were faster after CSDS in resilient mice specifically. In females, rod ERGs revealed age-related changes with no change in cone ERGs. Finally, our analysis suggests that baseline ERG can predict with an efficacy up to 71% the expression of susceptibility and resilience before stress exposition in males and females. Overall, our findings suggest that retinal activity is a valid biomarker of stress response that could potentially serve as a tool to predict whether males and females will become susceptible or resilient when facing CSDS.

scholarly journals Trajectories of Functional Health Following Stroke: The Role of Social Resources

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 847-847
Author(s):  
Takeshi Nakagawa ◽  
Taiji Noguchi ◽  
Ayane Komatsu ◽  
Masumi Ishihara ◽  
Tami Saito
Keyword(s):  
Social Participation ◽  
Functional Decline ◽  
Protective Role ◽  
Social Resources ◽  
Stroke Onset ◽  
Functional Health ◽  
Japanese Adults ◽  
Before And After ◽  
Crucial Information

Abstract Stroke is one of the major causes of disability in old age. Predictors for the functional prognosis have been studied, but the role of social resources in recovery has not studied as much. We examined whether social resources available before and after stroke onset improved functional prognoses. Data was derived from longitudinal data collected between 1987 and 2006 from Japanese adults aged 60 years and older. We identified 396 people who had experienced their self- or proxy-reported first stroke during follow-up (age at stroke onset: M = 76.0, SD = 6.9; 74.2% women). Functional health was measured by self- or proxy-reported activities of daily living. Social resources were indexed as residential status, contact with non-coresident children, social participation, and perceived support. Analyses were adjusted for age at stroke onset, gender, and education. A multiphase growth model showed that functional health typically deteriorated surrounding stroke and gradually declined thereafter. There were also individual differences in the trajectories of functional health. Individuals who more frequently participated in social groups prior to stroke and those who came to participate more frequently thereafter exhibited less functional decline immediately following stroke. Our findings indicate that social participation plays a protective role against adverse prognoses following stroke regardless of when individuals start participating. Inclusive communities would enable older adults to remain independent. Our study was limited in that crucial information about stroke, such as objective measures of initial severity, was not available and that individuals with more severe stroke may have dropped out after the onset.

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