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atherosclerosis and senescence

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https://www.readbyqxmd.com/read/29750567/cellular-senescence-links-aging-and-diabetes-in-cardiovascular-disease
#1
Hadis Shakeri, Katrien Lemmens, Andreas B Gevaert, Guido R Y De Meyer, Vincent Segers
Aging is a powerful independent risk factor for cardiovascular diseases such as atherosclerosis and heart failure. Concomitant diabetes mellitus strongly reinforces this effect of aging on cardiovascular disease. Cellular senescence is a fundamental mechanism of aging and appears to play a crucial role in the onset and prognosis of cardiovascular disease in the context of both aging and diabetes. Senescent cells are in a state of cell cycle arrest, but remain metabolically active by secreting inflammatory factors...
May 11, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29710840/nadph-oxidases-and-mitochondria-in-vascular-senescence
#2
REVIEW
Gloria Salazar
Aging is the major risk factor in the development of cardiovascular diseases (CVDs), including hypertension, atherosclerosis, and myocardial infarction. Oxidative stress caused by overproduction of reactive oxygen species (ROS) and/or by reduced expression of antioxidant enzymes is a major contributor to the progression of vascular senescence, pathologic remodeling of the vascular wall, and disease. Both oxidative stress and inflammation promote the development of senescence, a process by which cells stop proliferating and become dysfunctional...
April 29, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29695496/oxldl-mediated-cellular-senescence-is-associated-with-increased-nadph-oxidase-p47phox-recruitment-to-caveolae
#3
Jing Wang, Yuzhi Bai, Xia Zhao, Jing Ru, Ning Kang, Tian Tian, Liying Tang, Yun An, Pei Li
Atherosclerosis develops as a consequence of inflammation and cell senescence.  In critical factors involved in the atherosclerotic changes, reactive oxygen species (ROS) generation is considered a leading cause.  While NADPH oxidases, particularly NOX2, are the main source of ROS, how they are regulated in the disease is incompletely understood.  In addition, how caveolae, the membrane structure implicated in oxLDL deposition under vascular endothelia, is involved in the oxLDL mediated ROS production remains mostly elusive...
April 25, 2018: Bioscience Reports
https://www.readbyqxmd.com/read/29691578/-effects-of-thyroid-hormone-on-macrophage-dysfunction-induced-by-oxidized-low-density-lipoprotein
#4
Yu Ning, Ming Zhang, Yun-Hui DU, Hui-Na Zhang, Lin-Yi Li, Yan-Wen Qin, Wan-Wan Wen, Quan-Ming Zhao
It has been recognized that patients with hypothyroidism have higher risks of atherosclerosis and coronary heart disease, however, the mechanisms are largely unknown. Considering that macrophage dysfunction plays an important role in the formation and development of atherosclerosis plaques, this study aimed to investigate the direct effects of thyroid hormone on macrophage functions and to provide new insight for the mechanism of hypothyroid atherosclerosis. RAW264.7 cells (mouse leukaemic monocyte macrophage cell line) were incubated with oxidized low-density lipoprotein (oxLDL) to establish macrophage foam cells model in vitro, and the protective effects of different concentration of thyroxine (T4) on the macrophage foam cells function were explored...
April 25, 2018: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/29686666/age-and-age-related-diseases-role-of-inflammation-triggers-and-cytokines
#5
REVIEW
Irene Maeve Rea, David S Gibson, Victoria McGilligan, Susan E McNerlan, H Denis Alexander, Owen A Ross
Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging. This reshaping of cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called "inflamm-aging." Despite research there is no clear understanding about the causes of "inflamm-aging" that underpin most major age-related diseases, including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, cancer, and aging itself...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29682164/defective-autophagy-in-atherosclerosis-to-die-or-to-senesce
#6
REVIEW
Mandy O J Grootaert, Lynn Roth, Dorien M Schrijvers, Guido R Y De Meyer, Wim Martinet
Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles such as mitochondria (a process termed "mitophagy") via lysosomes. It is crucial for regulating protein and mitochondrial quality control and maintaining cellular homeostasis, whereas dysregulation of autophagy has been implicated in a wide range of diseases including atherosclerosis. Recent evidence has shown that the autophagic process becomes dysfunctional during the progression of atherosclerosis, regardless of whether there are many autophagy-stimulating factors (e...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29681573/amlodipine-inhibits-vascular-cell-senescence-and-protects-against-atherogenesis-through-the-mechanism-independent-of-calcium-channel-blockade
#7
Hiromi Kayamori, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Tohru Minamino
Vascular cells have a finite lifespan and eventually enter irreversible growth arrest called cellular senescence. We have previously suggested that vascular cell senescence contributes to the pathogenesis of human atherosclerosis. Amlodipine is a mixture of two enantiomers, one of which (S- enantiomer) has L-type channel blocking activity, while the other (R+ enantiomer) shows ~1000-fold weaker channel blocking activity than S- enantiomer and has other unknown effects. It has been reported that amlodipine inhibits the progression of atherosclerosis in humans, but the molecular mechanism of this beneficial effect remains unknown...
April 20, 2018: International Heart Journal
https://www.readbyqxmd.com/read/29643057/defective-base-excision-repair-of-oxidative-dna-damage-in-vascular-smooth-muscle-cells-promotes-atherosclerosis
#8
Aarti Shah, Kelly Gray, Nichola Figg, Alison Finigan, Lakshi Starks, Martin Bennett
Background -Atherosclerotic plaques demonstrate extensive accumulation of oxidative DNA damage, predominantly as 8-oxoguanine (8oxoG) lesions. 8oxoG is repaired by base excision repair (BER) enzymes; however, the mechanisms regulating 8oxoG accumulation in vascular smooth muscle cells (VSMCs) and its effects on their function and in atherosclerosis are unknown. Methods -We studied levels of 8oxoG and its regulatory enzymes in human atherosclerosis, the mechanisms regulating 8oxoG repair and the BER enzyme 8oxoG DNA glycosylase I (OGG1) in VSMCs in vitro, and the effects of reducing 8oxoG in VSMCs in atherosclerosis in ApoE-/- mice...
April 11, 2018: Circulation
https://www.readbyqxmd.com/read/29512862/microrna-216a-induces-endothelial-senescence-and-inflammation-via-smad3-i%C3%AE%C2%BAb%C3%AE-pathway
#9
Shujun Yang, Xuenan Mi, Yu Chen, Congrui Feng, Zhihui Hou, Rutai Hui, Weili Zhang
Vascular endothelial senescence contributes to atherosclerosis and coronary artery disease (CAD), but the mechanisms are yet to be clarified. We identified that microRNA-216a (miR-216a) significantly increased in senescent endothelial cells. The replicative senescence model of human umbilical vein endothelial cells (HUVECs) was established to explore the role of miR-216a in endothelial ageing and dysfunction. Luciferase assay indicated that Smad3 was a direct target of miR-216a. Stable expression of miR-216a induced a premature senescence-like phenotype in HUVECs with an impairment in proliferation and migration and led to an increased adhesion to monocytes by inhibiting Smad3 expression and thereafter modulating the degradation of NF-κB inhibitor alpha (IκBα) and activation of adhesion molecules...
May 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29449647/the-pro-inflammatory-phenotype-of-the-human-non-classical-monocyte-subset-is-attributed-to-senescence
#10
Siew-Min Ong, Eva Hadadi, Truong-Minh Dang, Wei-Hseun Yeap, Crystal Tze-Ying Tan, Tze-Pin Ng, Anis Larbi, Siew-Cheng Wong
Human primary monocytes comprise a heterogeneous population that can be classified into three subsets based on CD14 and CD16 expression: classical (CD14high /CD16- ), intermediate (CD14high /CD16+ ), and non-classical (CD14low /CD16+ ). The non-classical monocytes are the most pro-inflammatory in response to TLR stimulation in vitro, yet they express a remarkably high basal level of miR-146a, a microRNA known to negatively regulate the TLR pathway. This concurrence of a pro-inflammatory status and a high miR-146a level has been associated with cellular senescence in other cell types...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29425296/inhibiting-cellular-senescence-a-new-therapeutic-paradigm-for-age-related-osteoporosis
#11
Sundeep Khosla, Joshua N Farr, James L Kirkland
Context: With the aging of the population and projected increase in osteoporotic fractures, coupled with the declining use of osteoporosis medications, there is a compelling need for new approaches to treat osteoporosis. Given that age-related osteoporosis generally co-exists with multiple other co-morbidities (e.g., atherosclerosis, diabetes, frailty), all sharing aging itself as the leading risk factor, there is growing interest in the "Geroscience Hypothesis", which posits that manipulation of fundamental aging mechanisms will delay the appearance or severity of multiple chronic diseases because these diseases share the same underlying risk factor - age...
February 7, 2018: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/29415069/administration-of-l-arginine-plus-l-citrulline-or-l-citrulline-alone-successfully-retarded-endothelial-senescence
#12
Tomoe Tsuboi, Morihiko Maeda, Toshio Hayashi
L-citrulline and L-arginine supplementation has been shown to have several beneficial effects on the cardiovascular system. Nitric oxide (NO) protects against the progression of atherosclerosis and is synthesized by nitric oxide synthase (NOS), which converts L-arginine (L-Arg) into L-citrulline (L-Cit). Our previous study revealed that chronic administration of a combination of L-Cit and L- Arg has a better therapeutic effect on high cholesterol-induced atherosclerosis in rabbits. We investigated how L-Arg and L-Cit affect endothelial function, aging and atherosclerosis...
2018: PloS One
https://www.readbyqxmd.com/read/29360955/vascular-smooth-muscle-cell-death-autophagy-and-senescence-in-atherosclerosis
#13
Mandy O J Grootaert, Manon Moulis, Lynn Roth, Wim Martinet, Cécile Vindis, Martin R Bennett, Guido R Y De Meyer
In the present review, we describe the causes and consequences of loss of vascular smooth muscle cells (VSMCs) or their function in advanced atherosclerotic plaques and discuss possible mechanisms such as cell death or senescence, and induction of autophagy to promote cell survival. We also highlight the potential use of pharmacological modulators of these processes to limit plaque progression and/or improve plaque stability. VSMCs play a pivotal role in atherogenesis. Loss of VSMCs via initiation of cell death leads to fibrous cap thinning and promotes necrotic core formation and calcification...
March 15, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29359784/puerarin-protects-endothelial-progenitor-cells-from-damage-of-angiotensin-ii-via-activation-of-erk1-2%C3%A2-nrf2-signaling-pathway
#14
Chen Fu, Baoxin Chen, Xianglan Jin, Xuemei Liu, Fengli Wang, Rongjuan Guo, Zhigang Chen, Hong Zheng, Le Wang, Yunling Zhang
Endothelial progenitor cell (EPC) dysfunction is associated with the formation of carotid atherosclerosis. It has been demonstrated that angiotensin II (Ang II) may impair the function of EPCs and puerarin, a natural product, possesses cardiovascular protective effects against oxidative stress and inflammation. Therefore, the present study aimed to investigate the beneficial effects of puerarin in Ang II‑induced EPC injury, and to elucidate the underlying mechanisms. Treatment with Ang II suppressed EPC proliferation and migration, increased the expression of the senescence marker β‑galactosidase, and the adhesion molecules intracellular adhesion molecule‑1 and vascular cell adhesion molecule‑1...
March 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29300828/non-coding-rnas-key-regulators-of-smooth-muscle-cell-fate-in-vascular-disease
#15
Nicholas J Leeper, Lars Maegdefessel
The vascular smooth muscle cell (SMC) is one of the most plastic cells in the body. Understanding how non-coding RNAs (ncRNAs) regulate SMC cell-fate decision making in the vasculature has significantly enhanced our understanding of disease development, and opened up exciting new avenues for potential therapeutic applications. Recent studies on SMC physiology have in addition challenged our traditional view on their role and contribution to vascular disease, mainly in the setting of atherosclerosis as well as aneurysm disease, and restenosis after angioplasties...
March 15, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29289557/salidroside-attenuates-endothelial-cellular-senescence-via-decreasing-the-expression-of-inflammatory-cytokines-and-increasing-the-expression-of-sirt3
#16
Sha-Sha Xing, Jian Li, Lin Chen, Ya-Fei Yang, Ping-Lin He, Jun Li, Jin Yang
OBJECTIVE: Endothelial cellular senescence is an important contributor to the endothelial dysfunction and atherosclerosis. Our previous studies suggested that salidroside (SAL) can alleviate atherosclerosis and protect endothelial cells against oxidative stress induced damage. However, the effect and mechanism of SAL on endothelial cellular senescence is still unclear. Here, we investigated the underlying mechanisms of SAL on preventing endothelial cellular premature senescence. METHODS AND RESULTS: We established a hyperhomocysteinemia (HHcy)mouse model via high methionine diet (HMD) to explore the protective effect of SAL...
December 28, 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/29286156/metformin-induced-activation-of-ampk-inhibits-the-proliferation-and-migration-of-human-aortic-smooth-muscle-cells-through-upregulation-of-p53-and-ifi16
#17
Biao Hao, Yan Xiao, Fang Song, Xiangshu Long, Jing Huang, Maobo Tian, Shiyan Deng, Qiang Wu
The proliferation and migration of vascular smooth muscle cells are significant in the development and progression of atherosclerosis and plaque rupture. Metformin is a widely used antidiabetic drug, which has been reported to inhibit cell growth and migration. The antiproliferative and antimigratory effects of metformin have been attributed to 5' adenosine monophosphate-activated protein kinase (AMPK) activation. The purpose of the present study was to investigate the effects of metformin on primary human aortic muscle cells (HASMCs) in vitro and to clarify the underlying mechanism...
March 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29274344/calcium-phosphate-particles-stimulate-interleukin-1%C3%AE-release-from-human-vascular-smooth-muscle-cells-a-role-for-spleen-tyrosine-kinase-and-exosome-release
#18
Yana Dautova, Alexander N Kapustin, Kevin Pappert, Matthias Epple, Hanneke Okkenhaug, Simon J Cook, Catherine M Shanahan, Martin D Bootman, Diane Proudfoot
AIMS: Calcium phosphate (CaP) particle deposits are found in several inflammatory diseases including atherosclerosis and osteoarthritis. CaP, and other forms of crystals and particles, can promote inflammasome formation in macrophages leading to caspase-1 activation and secretion of mature interleukin-1β (IL-1β). Given the close association of small CaP particles with vascular smooth muscle cells (VSMCs) in atherosclerotic fibrous caps, we aimed to determine if CaP particles affected pro-inflammatory signalling in human VSMCs...
February 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29259496/immunosenescence-in-aging-between-immune-cells-depletion-and-cytokines-up-regulation
#19
REVIEW
Maria Teresa Ventura, Marco Casciaro, Sebastiano Gangemi, Rosalba Buquicchio
Background: The immunosenescence is a relatively recent chapter, correlated with the linear extension of the average life began in the nineteenth century and still in progress. The most important feature of immunosenescence is the accumulation in the "immunological space" of memory and effector cells as a result of the stimulation caused by repeated clinical and subclinical infections and by continuous exposure to antigens (inhalant allergens, food, etc.). This state of chronic inflammation that characterizes senescence has a significant impact on survival and fragility...
2017: Clinical and Molecular Allergy: CMA
https://www.readbyqxmd.com/read/29247791/immune-senescence-and-biomarkers-profile-of-bambu%C3%A3-aged-population-based-cohort
#20
Karen Cecília Lima Torres, Vitor Bortolo de Rezende, Maria Luiza Lima-Silva, Lorena Júnia de Souza Santos, Carla Gabriela Costa, Juliana Vaz de Melo Mambrini, Sérgio Viana Peixoto, Eduardo Tarazona-Santos, Olindo Assis Martins Filho, Maria Fernanda Lima-Costa, Andréa Teixeira-Carvalho
During immunosenescence many proinflammatory markers such as cytokines and chemokines are increased. This process called by Franceschi and colleagues as inflammaging is associated with chronic inflammation and the ethiology and pathophysiolgy of many ageing diseases as Alzheimer's and atherosclerosis. The knowledge of immune profile during ageing may provide some interventions that would improve the immune function in elderly and quality of life for old people. However, the identification of a group of potential biomarkers to monitor the ageing process is very difficult...
March 2018: Experimental Gerontology
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