scholarly journals P4-648: AEROBIC FITNESS ATTENUATES AGE-RELATED RISK OF CARDIOVASCULAR DISEASE

2019 ◽  
Vol 15 ◽  
pp. P1577-P1578
Author(s):  
Colleen Mellert ◽  
Sarah Lose ◽  
Chuck Illingworth ◽  
Jennifer M. Oh ◽  
Allen Wenzel ◽  
...  
2008 ◽  
Vol 105 (5) ◽  
pp. 1628-1631 ◽  
Author(s):  
Giovanni G. Camici ◽  
Francesco Cosentino ◽  
Felix C. Tanner ◽  
Thomas F. Lüscher

Accumulation of oxidative stress with age is hypothesized to be the primary causative mediator of age-associated diseases. Among different tissues, aging vessels are known to accumulate oxidative damage and undergo functional impairment. Oxidative stress affects the availability and/or balance of key regulators of vascular homeostasis and favors the development of cardiovascular disease. Reactive oxygen species are generated by different intracellular molecular pathways principally located in the cytoplasm and in the mitochondria. The mitochondrial enzyme p66Shc is an adaptor protein and plays an important role as a redox enzyme implicated in mitochondrial eactive oxygen species generation and translation of oxidative signals into apoptosis. Mice lacking p66Shc−/− gene display reduced production of intracellular oxidants and a 30% prolonged life span. For this reasons, a series of studies conceived to elucidate the function of p66Shc and its possible implication in age-associated cardiovascular diseases have been carried out. Indeed, p66Shc−/− mice have been shown to be protected from age-dependent endothelial dysfunction as well as age-related risk factors such as diabetes and hypercholesterolemia. This review focuses on delineating the role of the p66Shc adaptor protein and its potential implication in the pathophysiology of aging and age-related cardiovascular disease.


2020 ◽  
Author(s):  
Chunmei Xie ◽  
De Chang ◽  
Linhai Li ◽  
Xiaohua Peng ◽  
Zhijian Ling ◽  
...  

2012 ◽  
Vol 19 (2) ◽  
pp. 85-92
Author(s):  
Renata Giudice ◽  
Raffaele Izzo ◽  
Maria Virgina Manzi ◽  
Giampiero Pagnano ◽  
Mario Santoro ◽  
...  

Author(s):  
Spencer W. Liebel ◽  
Lawrence H. Sweet

Cardiovascular disease (CVD) affects approximately 44 million American adults older than age 60 years and remains the leading cause of death in the United States, with approximately 610,000 each year. With improved survival from acute cardiac events, older adults are often faced with the prospect of living with CVD, which causes significant psychological, social, and economic hardship. The various disease processes that constitute CVD also exert a deleterious effect on neurocognitive functioning. Although existing knowledge of neurocognitive functioning in CVD and its subtypes is substantial, a review of these findings by CVD type and neurocognitive domain does not exist, despite the potential impact of this information for patients, health care providers, and clinical researchers. This chapter provides a resource for clinicians and researchers on the epidemiology, mechanisms, and neurocognitive effects of CVDs. This chapter includes a discussion of neurocognitive consequences of CVD subtypes by neuropsychological domain and recommendations for assessment. Overall, the CVD subtypes that have the most findings available on specific neurocognitive domains are heart failure, hypertension, and atrial fibrillation. Despite a large discrepancy between the number of available studies across CVD subtypes, existing literature on neurocognitive effects by domain is consistent with the literature on the neurocognitive sequelae of unspecified CVD. Specifically, the research literature suggests that cognitive processing speed, attention, executive functioning, and memory are the domains most frequently affected. Given the prevalence of CVDs, neuropsychological assessment of older adults should include instruments that allow consideration of these potential neurocognitive consequences of CVD.


2021 ◽  
Vol 22 (15) ◽  
pp. 7797
Author(s):  
Joseph A. M. J. L. Janssen

For many years, the dogma has been that insulin resistance precedes the development of hyperinsulinemia. However, recent data suggest a reverse order and place hyperinsulinemia mechanistically upstream of insulin resistance. Genetic background, consumption of the “modern” Western diet and over-nutrition may increase insulin secretion, decrease insulin pulses and/or reduce hepatic insulin clearance, thereby causing hyperinsulinemia. Hyperinsulinemia disturbs the balance of the insulin–GH–IGF axis and shifts the insulin : GH ratio towards insulin and away from GH. This insulin–GH shift promotes energy storage and lipid synthesis and hinders lipid breakdown, resulting in obesity due to higher fat accumulation and lower energy expenditure. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, cancer and premature mortality. It has been further hypothesized that nutritionally driven insulin exposure controls the rate of mammalian aging. Interventions that normalize/reduce plasma insulin concentrations might play a key role in the prevention and treatment of age-related decline, obesity, type 2 diabetes, cardiovascular disease and cancer. Caloric restriction, increasing hepatic insulin clearance and maximizing insulin sensitivity are at present the three main strategies available for managing hyperinsulinemia. This may slow down age-related physiological decline and prevent age-related diseases. Drugs that reduce insulin (hyper) secretion, normalize pulsatile insulin secretion and/or increase hepatic insulin clearance may also have the potential to prevent or delay the progression of hyperinsulinemia-mediated diseases. Future research should focus on new strategies to minimize hyperinsulinemia at an early stage, aiming at successfully preventing and treating hyperinsulinemia-mediated diseases.


2008 ◽  
Vol 92 (4) ◽  
pp. 509-512 ◽  
Author(s):  
J S L Tan ◽  
J J Wang ◽  
G Liew ◽  
E Rochtchina ◽  
P Mitchell

2021 ◽  
Vol 22 (18) ◽  
pp. 9867
Author(s):  
Yi-Chun Huang ◽  
Chao-Yung Wang

Clinical evidence suggests that conventional cardiovascular disease (CVD) risk factors cannot explain all CVD incidences. Recent studies have shown that telomere attrition, clonal hematopoiesis of indeterminate potential (CHIP), and atherosclerosis (telomere–CHIP–atherosclerosis, TCA) evolve to play a crucial role in CVD. Telomere dynamics and telomerase have an important relationship with age-related CVD. Telomere attrition is associated with CHIP. CHIP is commonly observed in elderly patients. It is characterized by an increase in blood cell clones with somatic mutations, resulting in an increased risk of hematological cancer and atherosclerotic CVD. The most common gene mutations are DNA methyltransferase 3 alpha (DNMT3A), Tet methylcytosine dioxygenase 2 (TET2), and additional sex combs-like 1 (ASXL1). Telomeres, CHIP, and atherosclerosis increase chronic inflammation and proinflammatory cytokine expression. Currently, their epidemiology and detailed mechanisms related to the TCA axis remain incompletely understood. In this article, we reviewed recent research results regarding the development of telomeres and CHIP and their relationship with atherosclerotic CVD.


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