scholarly journals The Ageing Endothelium

2021 ◽  
Author(s):  
Ka Ka Ting ◽  
Paul Coleman ◽  
Yang Zhao ◽  
Mathew A Vadas ◽  
Jennifer R Gamble
Keyword(s):  
Chronic Diseases ◽  
Cellular Senescence ◽  
Vascular Endothelium ◽  
Vascular Diseases ◽  
Therapeutic Strategies ◽  
Metabolic Changes ◽  
Age Related

Cellular senescence is now recognised as one of the hallmarks of ageing. Herein, we examine current findings on senescence of the vascular endothelium and its impacts on age-related vascular diseases. Endothelial senescence can result in systemic metabolic changes, implicating senescence in chronic diseases such as diabetes, obesity and atherosclerosis. Senolytics, drugs that eliminate senescent cells, afford new therapeutic strategies for control of these chronic diseases.

scholarly journals Nrf2 dysfunction and impaired cellular resilience to oxidative stressors in the aged vasculature: from increased cellular senescence to the pathogenesis of age-related vascular diseases

GeroScience ◽  
2019 ◽  
Vol 41 (6) ◽  
pp. 727-738 ◽  
Author(s):  
Zoltan Ungvari ◽  
Stefano Tarantini ◽  
Ádám Nyúl-Tóth ◽  
Tamas Kiss ◽  
Andriy Yabluchanskiy ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Vascular Diseases ◽  
Age Related ◽  
Cellular Resilience

scholarly journals Protective Role of Polyphenols against Vascular Inflammation, Aging and Cardiovascular Disease

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 53 ◽  
Author(s):  
Alexa Serino ◽  
Gloria Salazar
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Diseases ◽  
Cellular Senescence ◽  
Cellular Damage ◽  
Surrounding Tissue ◽  
Low Grade ◽  
Age Related ◽  
Extracellular Matrix Components ◽  
And Oxidative Stress

Aging is a major risk factor in the development of chronic diseases affecting various tissues including the cardiovascular system, muscle and bones. Age-related diseases are a consequence of the accumulation of cellular damage and reduced activity of protective stress response pathways leading to low-grade systemic inflammation and oxidative stress. Both inflammation and oxidative stress are major contributors to cellular senescence, a process in which cells stop proliferating and become dysfunctional by secreting inflammatory molecules, reactive oxygen species (ROS) and extracellular matrix components that cause inflammation and senescence in the surrounding tissue. This process is known as the senescence associated secretory phenotype (SASP). Thus, accumulation of senescent cells over time promotes the development of age-related diseases, in part through the SASP. Polyphenols, rich in fruits and vegetables, possess antioxidant and anti-inflammatory activities associated with protective effects against major chronic diseases, such as cardiovascular disease (CVD). In this review, we discuss molecular mechanisms by which polyphenols improve anti-oxidant capacity, mitochondrial function and autophagy, while reducing oxidative stress, inflammation and cellular senescence in vascular smooth muscle cells (VSMCs) and endothelial cells (ECs). We also discuss the therapeutic potential of polyphenols in reducing the effects of the SASP and the incidence of CVD.

scholarly journals Gene Expression, Oxidative Stress, and Senescence of Primary Coronary Endothelial Cells Exposed to Postprandial Serum of Healthy Adult and Elderly Volunteers after Oven-Cooked Meat Meals

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Costarelli Laura ◽  
Giacconi Robertina ◽  
Francesco Piacenza ◽  
Andrea Basso ◽  
Deborah Pacetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cellular Senescence ◽  
Plasma Lipids ◽  
Vascular Diseases ◽  
Epidemiological Studies ◽  
Human Coronary Artery ◽  
Meat Meal ◽  
Age Related ◽  
Expression Pathways

Epidemiological studies have linked high consumption of meat with major age-related diseases including cardiovascular diseases. Abnormal postprandial increases in plasma lipids after a meat meal have been hypothesized among the pathogenetic mechanisms. However, it is still unknown if the postprandial serum derived after a normal meat meal is able to affect endothelial function, and if the type of meat and the age of the donors are critical factors. Here, we show the effects of postprandial sera derived from healthy adults and elderly volunteers who consumed meat meals on human coronary artery endothelial cell (HCAEC) oxidative stress, gene expression, DNA damage, and cellular senescence. We observed that a single exposure to postprandial serum induces a slight increase in ROS that is associated with modulation of gene expression pathways related to oxidative stress response and metabolism. The postprandial-induced increase in ROS is not associated with a measurable DNA oxidative damage. However, repeated exposure to postprandial serum induces an acceleration of cellular senescence. Taking into account the deleterious role of cellular senescence in age-related vascular diseases, the results suggest a new mechanism by which excessive meat consumption and time spent in postprandial state may affect health status during aging.

Cellular senescence and the senescent secretory phenotype in age-related chronic diseases

2014 ◽  
Vol 17 (4) ◽  
pp. 324-328 ◽  
Author(s):  
Yi Zhu ◽  
Jacqueline L. Armstrong ◽  
Tamara Tchkonia ◽  
James L. Kirkland
Keyword(s):  
Chronic Diseases ◽  
Cellular Senescence ◽  
Age Related ◽  
Secretory Phenotype

scholarly journals The Senescence-Associated Secretory Phenotype (SASP) in the Challenging Future of Cancer Therapy and Age-Related Diseases

Biology ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 485
Author(s):  
Lorenzo Cuollo ◽  
Fabrizio Antonangeli ◽  
Angela Santoni ◽  
Alessandra Soriani
Keyword(s):  
Cancer Therapy ◽  
Molecular Mechanisms ◽  
Therapeutic Strategies ◽  
Senescent Cell ◽  
Pharmacological Intervention ◽  
Tissue Microenvironment ◽  
Age Related ◽  
Secretory Phenotype ◽  
Novel Therapeutic Strategies ◽  
Novel Therapeutic

Cellular senescence represents a robust tumor-protecting mechanism that halts the proliferation of stressed or premalignant cells. However, this state of stable proliferative arrest is accompanied by the Senescence-Associated Secretory Phenotype (SASP), which entails the copious secretion of proinflammatory signals in the tissue microenvironment and contributes to age-related conditions, including, paradoxically, cancer. Novel therapeutic strategies aim at eliminating senescent cells with the use of senolytics or abolishing the SASP without killing the senescent cell with the use of the so-called “senomorphics”. In addition, recent works demonstrate the possibility of modifying the composition of the secretome by genetic or pharmacological intervention. The purpose is not to renounce the potent immunostimulatory nature of SASP, but rather learning to modulate it for combating cancer and other age-related diseases. This review describes the main molecular mechanisms regulating the SASP and reports the evidence of the feasibility of abrogating or modulating the SASP, discussing the possible implications of both strategies.

scholarly journals Age-Related Chronic Diseases and Alzheimer’s Disease in Texas: A Hispanic Focused Study

2021 ◽  
Vol 5 (1) ◽  
pp. 121-133
Author(s):  
Shyam Sheladia ◽  
P. Hemachandra Reddy
Keyword(s):  
United States ◽  
Risk Factors ◽  
Chronic Diseases ◽  
Hispanic Americans ◽  
The United States ◽  
Modifiable Risk Factors ◽  
American Population ◽  
Hispanic American ◽  
West Texas ◽  
Age Related

The emergence of age-related chronic diseases within the United States has led to the direct increase of Alzheimer’s disease (AD) as well as other neurological diseases which ultimately contribute to the development of dementia within the general population. To be specific, age-related chronic diseases such as cardiovascular disease, high cholesterol, diabetes, and kidney disease contribute greatly to the advancement and rapid progression of dementia. Furthermore, unmodifiable risk factors such as advancing age and genetics as well as modifiable risk factors such as socioeconomic status, educational attainment, exercise, and diet further contribute to the development of dementia. Current statistics and research show that minority populations such as Hispanic Americans in the United States face the greatest burden of dementia due to the increase in the prevalence of overall population age, predisposing genetics, age-related chronic diseases, low socioeconomic status, as well as poor lifestyle choices and habits. Additionally, Hispanic Americans living within Texas and the rural areas of West Texas face the added challenge of finding appropriate healthcare services. This article will focus upon the research associated with AD as well as the prevalence of AD within the Hispanic American population of Texas and rural West Texas. Furthermore, this article will also discuss the prevalence of age-related chronic diseases, unmodifiable risk factors, and modifiable risk factors which lead to the progression and development of AD within the Hispanic American population of the United States, Texas, and rural West Texas.

scholarly journals Cellular Senescence in Lung Fibrosis

2021 ◽  
Vol 22 (13) ◽  
pp. 7012
Author(s):  
Fernanda Hernandez-Gonzalez ◽  
Rosa Faner ◽  
Mauricio Rojas ◽  
Alvar Agustí ◽  
Manuel Serrano ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cellular Senescence ◽  
Lung Fibrosis ◽  
Lung Diseases ◽  
Physiological Mechanism ◽  
Lung Parenchyma ◽  
Scar Tissue ◽  
Interstitial Lung Diseases ◽  
Cellular Damage ◽  
Age Related

Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.

scholarly journals Cellular Senescence and Mammalian Healthspan

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 742-742
Author(s):  
Judith Campisi
Keyword(s):  
Growth Factors ◽  
Cell Fate ◽  
Cellular Senescence ◽  
Complex Cell ◽  
Transgenic Mouse Models ◽  
Bioactive Lipids ◽  
Age Related ◽  
Mammalian Tissues ◽  
Secretory Phenotype ◽  
Near Future

Abstract Cellular senescence is a complex cell fate, often induced by stress or damage, that can be beneficial or deleterious, depending on the physiological context and age of the organism. A prominent feature of senescent cells is a multi-faceted senescence-associated secretory phenotype (SASP), which includes growth factors, cytokine and chemokines, growth factors, proteases, bioactive lipids and metabolites. Senescent cells increase with age in most, if not all, mammalian tissues. Through the use of transgenic mouse models, senescent cells are now known to causally drive numerous age-related pathologies, largely through the SASP. Eliminating senescent cells, genetically or through the use of senolytic/senomorphic agents, can improve the health span, at least in mice, and hold promise for extension to humans in the near future.

scholarly journals Dendranthema zawadskii var. lucidum (Nakai) J.H. Park Extract Inhibits Cellular Senescence in Human Dermal Fibroblasts and Aging-Related Inflammation in Rats

Processes ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 801
Author(s):  
Jehun Choi ◽  
Gwi-Yeong Jang ◽  
Jeonghoon Lee ◽  
Hae-Young Chung ◽  
Hyung-Jun Noh ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Cell Cycle Progression ◽  
Inflammatory Responses ◽  
Dermal Fibroblast ◽  
Dermal Fibroblasts ◽  
Dependent Manner ◽  
Aged Rats ◽  
Age Related ◽  
Dendranthema Zawadskii ◽  
Beta Galactosidase

Senescence is the phenomenon by which physiological functions of organisms degenerate with time. Cellular senescence is marked by an inhibition of cell cycle progression. Beta-galactosidase accumulates in the lysosomes of aged cells. In this study, human dermal fibroblast cells (HDFs) were treated with 0.5 μM doxorubicin for 4 h to induce cellular senescence. Senescence-associated beta-galactosidase (SA-β-gal) activity was then measured 72 h after treatment with aerial parts of Dendranthema zawadskii var. lucidum (Nakai) J.H. Park (DZ) extract. Treatment with DZ extract significantly decreased SA-β-gal activity in a dose-dependent manner in HDFs. Additionally, DZ extract treatment reduced age-related oxidative stress and inflammation in the aortas of aged rats. The reactive oxygen species (ROS) levels in aortas of aged control rats were higher than those in young rats. However, DZ extract-fed aged rats showed significantly lower ROS levels than the aged control rats. When the aged rats were treated with DZ extract at either 0.2 or 1.0 mg∙kg−1∙day−1, NF-κB levels in aorta tissue decreased significantly compared to those in aorta tissue of the aged control rats without DZ treatment. In addition, DZ extract-fed aged rat aortas showed significant reductions in expression of iNOS and COX-2 induced by NF-κB translocation. Therefore, these results suggest that DZ effectively inhibited senescence-related NF-κB activation and inflammation. DZ extract may have a role in the prevention of the vascular inflammatory responses that occur during vascular aging.

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