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Alzheimer’s disease (AD) represents the most common form of dementia in the elderly population worldwide. AD is characterized by progressive neurodegeneration that leads to a gradual deterioration of memory and other cognitive functions. Given the global prevalence and impact of AD, there is a critical need to establish biomarkers that can be used to detect AD in individuals before the onset of clinical signs and provide mitigating therapeutics. The aim of this Special Issue is to discuss the current knowledge as well as future perspectives on the role of biomarkers in the screening, diagnosis, treatment and follow-up of AD.
Medicine --- flotillin --- Alzheimer's disease --- biomarker --- exosomes --- beta-amyloid --- Tau --- aging --- biomarkers --- cytokines --- cognitive decline --- metabolomics --- neuroinflammation --- multivariate analysis --- physical performance --- person-tailored --- PET/CT --- (18F)FDG --- neuropsychological assessment --- APP mutations --- APOE alleles --- PSEN1 --- PSEN2 --- germline mutations --- late onset AD --- early onset AD --- familial AD --- genetics of AD --- mitochondrial spare respiratory capacity --- mitochondrial --- membrane potential --- glycolytic reserve --- semantic memory --- phonemic fluency --- episodic memory --- neuropsychology --- neuroimaging --- Alzheimer's disease --- mild cognitive impairment --- EEG --- TMS --- obesity --- diabetes --- inflammation --- Amyloid Beta --- mitochondrial dysfunction --- nutrition --- omega-3 fatty acids --- antioxidant --- carotenoids --- vitamin E --- cognition --- older adults --- ageing --- subjective cognitive decline --- clock genes --- Clock --- ApoE --- cardiovascular risk factors --- Alzheimer disease --- semantic priming --- amyloid beta --- cerebrospinal fluid --- amyloid beta peptide --- total tau --- phosphorylated tau --- diagnosis --- drug development --- clinical trials --- diagnostic research --- virus --- bacteria --- dementia --- blood --- behavioral and psychological symptoms of dementia (BPSD) --- Alzheimer's disease (AD) --- neuropsychiatry inventory scale (NPI) --- endophenotypes --- CART analysis --- MTHFR --- APOE --- COMT --- genetic variants --- early diagnosis --- biofluids --- amyloid cascade hypothesis --- glucose metabolism --- adipose tissue dysfunction --- energetic metabolism --- lysosomes dysfunction --- Type-3-Diabetes --- neurodegeneration --- amyloid --- tau --- soluble TREM2 --- NfL --- Multiplex --- SiMoA --- diagnostics --- messenger RNA --- microRNA --- neurotropic microbes --- precision medicine --- prognostics --- synaptic biomarkers --- neurofilament light chain --- flotillin --- Alzheimer's disease --- biomarker --- exosomes --- beta-amyloid --- Tau --- aging --- biomarkers --- cytokines --- cognitive decline --- metabolomics --- neuroinflammation --- multivariate analysis --- physical performance --- person-tailored --- PET/CT --- (18F)FDG --- neuropsychological assessment --- APP mutations --- APOE alleles --- PSEN1 --- PSEN2 --- germline mutations --- late onset AD --- early onset AD --- familial AD --- genetics of AD --- mitochondrial spare respiratory capacity --- mitochondrial --- membrane potential --- glycolytic reserve --- semantic memory --- phonemic fluency --- episodic memory --- neuropsychology --- neuroimaging --- Alzheimer's disease --- mild cognitive impairment --- EEG --- TMS --- obesity --- diabetes --- inflammation --- Amyloid Beta --- mitochondrial dysfunction --- nutrition --- omega-3 fatty acids --- antioxidant --- carotenoids --- vitamin E --- cognition --- older adults --- ageing --- subjective cognitive decline --- clock genes --- Clock --- ApoE --- cardiovascular risk factors --- Alzheimer disease --- semantic priming --- amyloid beta --- cerebrospinal fluid --- amyloid beta peptide --- total tau --- phosphorylated tau --- diagnosis --- drug development --- clinical trials --- diagnostic research --- virus --- bacteria --- dementia --- blood --- behavioral and psychological symptoms of dementia (BPSD) --- Alzheimer's disease (AD) --- neuropsychiatry inventory scale (NPI) --- endophenotypes --- CART analysis --- MTHFR --- APOE --- COMT --- genetic variants --- early diagnosis --- biofluids --- amyloid cascade hypothesis --- glucose metabolism --- adipose tissue dysfunction --- energetic metabolism --- lysosomes dysfunction --- Type-3-Diabetes --- neurodegeneration --- amyloid --- tau --- soluble TREM2 --- NfL --- Multiplex --- SiMoA --- diagnostics --- messenger RNA --- microRNA --- neurotropic microbes --- precision medicine --- prognostics --- synaptic biomarkers --- neurofilament light chain
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In the last two decades, due to the continuous increase of lifespans in Westernsocieties, and the consequent growing of the elderly population, have witnessedan increase in the number of studies on biological and molecular factors able topromote healthy aging and reach longevity. The study of the genetic componentof human longevity demonstrated that it accounts for 25% of intra populationphenotype variance. The efforts made to characterize the genetic determinantssuggested that the maintenance of cellular integrity, inflammation, oxidativestress response, DNA repair, as well as the use of nutrients, represent the mostimportant pathways correlated with a longer lifespan. However, although aplethora of variants were indicated to be associated with human longevity, onlyvery few were successfully replicated in different populations, probably becauseof population specificity, missing heritability as well as a complex interactionamong genetic factors with lifestyle and cultural factors, which modulate theindividual chance of living longer. Thus, many challenges remain to be addressedin the search for the genetic components of human longevity. This Special Issue isaimed to unify the progress in the analysis of the genetic determinants of humanlongevity, to take stock of the situation and point to future directions of the field.We invite submissions for reviews, research articles, short-communicationsdealing with genetic association studies in human longevity, including all types ofgenetic variation, as well as the characterization of longevity-related genes.
unknown zygosity --- exceptional longevity --- TERC --- xenobiotic-metabolizing enzymes --- lifespan --- gender-specific association --- long-livers --- polymorphism --- cumulative incidence curves --- cardiovascular health --- twins --- genetic determinants of human longevity --- TERT --- SNP --- moonlighting protein --- longevity --- genomics --- APOE --- polygenic risk score --- signal transduction --- xenobiotics --- survival --- IPMK --- genetic variation --- genetic association study --- molecular senescence --- zygosity --- longevity-related genes --- age-stratification --- lipid profile --- mortality --- apolipoprotein E --- aging --- model systems --- leukocyte telomere length --- inositol phosphates --- human lifespan --- populations
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Alzheimer’s disease (AD) represents the most common form of dementia in the elderly population worldwide. AD is characterized by progressive neurodegeneration that leads to a gradual deterioration of memory and other cognitive functions. Given the global prevalence and impact of AD, there is a critical need to establish biomarkers that can be used to detect AD in individuals before the onset of clinical signs and provide mitigating therapeutics. The aim of this Special Issue is to discuss the current knowledge as well as future perspectives on the role of biomarkers in the screening, diagnosis, treatment and follow-up of AD.
flotillin --- Alzheimer’s disease --- biomarker --- exosomes --- beta-amyloid --- Tau --- aging --- biomarkers --- cytokines --- cognitive decline --- metabolomics --- neuroinflammation --- multivariate analysis --- physical performance --- person-tailored --- PET/CT --- (18F)FDG --- neuropsychological assessment --- APP mutations --- APOE alleles --- PSEN1 --- PSEN2 --- germline mutations --- late onset AD --- early onset AD --- familial AD --- genetics of AD --- mitochondrial spare respiratory capacity --- mitochondrial --- membrane potential --- glycolytic reserve --- semantic memory --- phonemic fluency --- episodic memory --- neuropsychology --- neuroimaging --- Alzheimer's disease --- mild cognitive impairment --- EEG --- TMS --- obesity --- diabetes --- inflammation --- Amyloid Beta --- mitochondrial dysfunction --- nutrition --- omega-3 fatty acids --- antioxidant --- carotenoids --- vitamin E --- cognition --- older adults --- ageing --- subjective cognitive decline --- clock genes --- Clock --- ApoE --- cardiovascular risk factors --- Alzheimer disease --- semantic priming --- amyloid beta --- cerebrospinal fluid --- amyloid beta peptide --- total tau --- phosphorylated tau --- diagnosis --- drug development --- clinical trials --- diagnostic research --- virus --- bacteria --- dementia --- blood --- behavioral and psychological symptoms of dementia (BPSD) --- Alzheimer’s disease (AD) --- neuropsychiatry inventory scale (NPI) --- endophenotypes --- CART analysis --- MTHFR --- APOE --- COMT --- genetic variants --- early diagnosis --- biofluids --- amyloid cascade hypothesis --- glucose metabolism --- adipose tissue dysfunction --- energetic metabolism --- lysosomes dysfunction --- Type-3-Diabetes --- neurodegeneration --- amyloid --- tau --- soluble TREM2 --- NfL --- Multiplex --- SiMoA --- diagnostics --- messenger RNA --- microRNA --- neurotropic microbes --- precision medicine --- prognostics --- synaptic biomarkers --- neurofilament light chain --- n/a --- Alzheimer's disease (AD)
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Down syndrome (DS), caused by the triplication of chromosome 21, is the most common genetic cause of intellectual disability (ID). Individuals with DS commonly exhibit unique neuropsychological profiles that emerge during specific developmental stages across the lifespan, often characterized by early developmental delay, cognitive strengths and weaknesses, behavior and mental health issues, and age-related cognitive decline, frequently resulting in early-onset Alzheimer’s disease. These profiles are unique compared to other individuals with ID and reflect the genetic mechanisms and neuroanatomic features underlying the distinct neuropsychological phenotype associated with DS. This Special Issue aims to highlight the recent advancements in understanding the neuropsychological phenotype associated with DS across the lifespan. The lifespan perspective will cover four developmental stages: (1) early childhood; (2) school age; (3) young adulthood, and (4) older adulthood. Authors contributed cutting-edge original research studies and comprehensive reviews that address a broad range of topics related to DS, including early developmental trajectories, cognitive functioning, language, adaptive skills, behavior and mental health, assessment and diagnosis, age-related cognitive decline, and medical issues related to the neuropsychological phenotype and neuroimaging.
trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer’s disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence --- n/a --- Alzheimer's disease
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Although regular moderate-intensity exercise can activate important cell adaptive properties, sporadic and strenuous bouts of exercise may induce oxidative stress due to an augmented production of reactive metabolites of oxygen (ROS) and nitrogen free radical species (RNS). Exercise-induced free radical formation may impair cell function by oxidatively modifying nucleic acids, where DNA damage and insufficient repair may lead to genomic instability. Likewise, lipid and protein damage are significant cellular events that can elicit potentially toxic perturbations in cellular homeostasis. This book focuses on aspects of exercise-induced oxidative stress while taking into consideration the basic mechanisms, consequences and function of ROS production, and whether antioxidants may either support or hinder these responses.
ApoE --- exercise --- antioxidants --- oxidative stress --- cognition --- motor --- vitamin E --- vitamin C --- aging --- Alzheimer’s disease --- lymphocytes --- mitochondrial transmembrane potential decline --- thiobarbituric acid reactive substance --- protein carbonyl --- skeletal muscle --- obesity --- fatigue --- diazoxide --- catalase --- superoxide dismutase --- oxidized glutathione --- reduced glutathione --- hemoglobin --- power output --- eccentric exercise --- redox status --- erythrocyte --- metabolism --- probiotics --- physical exercise --- male cyclists --- oxidative stress biomarkers --- antioxidative enzymes --- ultraendurance exercise --- muscle injury --- diet --- reactive oxygen species --- adipose tissue --- antioxidant supplement --- circadian rhythms --- reactive oxygen and nitrogen species (RONS) --- exercise training --- antioxidant --- n/a --- Alzheimer's disease
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Down syndrome (DS), caused by the triplication of chromosome 21, is the most common genetic cause of intellectual disability (ID). Individuals with DS commonly exhibit unique neuropsychological profiles that emerge during specific developmental stages across the lifespan, often characterized by early developmental delay, cognitive strengths and weaknesses, behavior and mental health issues, and age-related cognitive decline, frequently resulting in early-onset Alzheimer’s disease. These profiles are unique compared to other individuals with ID and reflect the genetic mechanisms and neuroanatomic features underlying the distinct neuropsychological phenotype associated with DS. This Special Issue aims to highlight the recent advancements in understanding the neuropsychological phenotype associated with DS across the lifespan. The lifespan perspective will cover four developmental stages: (1) early childhood; (2) school age; (3) young adulthood, and (4) older adulthood. Authors contributed cutting-edge original research studies and comprehensive reviews that address a broad range of topics related to DS, including early developmental trajectories, cognitive functioning, language, adaptive skills, behavior and mental health, assessment and diagnosis, age-related cognitive decline, and medical issues related to the neuropsychological phenotype and neuroimaging.
Medicine --- Neurosciences --- trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer's disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence --- trisomy 21 --- decoding --- vocabulary --- letters --- phonological awareness --- down syndrome --- fluency --- disfluency --- co-occurrence --- comorbidity --- language --- Down syndrome --- social cognition --- social behavior --- measurement --- children --- attention --- audiovisual processing --- communicative abilities in infants --- Trisomy 21 --- independence --- transition to adulthood --- proxy-report --- regression --- Alzheimer's disease --- biomarkers --- dementia --- cognition --- functional independence --- neuropsychological assessment --- primary care --- screening --- early regression --- idiopathic regression --- depression --- selective serotonin reuptake inhibitor --- mild cognitive impairment --- cognitive decline --- neuropsychological tests --- cognitive function --- early-onset Alzheimer disease --- late-onset Alzheimer disease --- hypothyroidism --- thyroid autoantibodies --- TSH --- Free T4 --- APOE Ɛ4 --- autism spectrum disorder --- co-occurring --- prevalence
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Although regular moderate-intensity exercise can activate important cell adaptive properties, sporadic and strenuous bouts of exercise may induce oxidative stress due to an augmented production of reactive metabolites of oxygen (ROS) and nitrogen free radical species (RNS). Exercise-induced free radical formation may impair cell function by oxidatively modifying nucleic acids, where DNA damage and insufficient repair may lead to genomic instability. Likewise, lipid and protein damage are significant cellular events that can elicit potentially toxic perturbations in cellular homeostasis. This book focuses on aspects of exercise-induced oxidative stress while taking into consideration the basic mechanisms, consequences and function of ROS production, and whether antioxidants may either support or hinder these responses.
Research & information: general --- Biology, life sciences --- ApoE --- exercise --- antioxidants --- oxidative stress --- cognition --- motor --- vitamin E --- vitamin C --- aging --- Alzheimer's disease --- lymphocytes --- mitochondrial transmembrane potential decline --- thiobarbituric acid reactive substance --- protein carbonyl --- skeletal muscle --- obesity --- fatigue --- diazoxide --- catalase --- superoxide dismutase --- oxidized glutathione --- reduced glutathione --- hemoglobin --- power output --- eccentric exercise --- redox status --- erythrocyte --- metabolism --- probiotics --- physical exercise --- male cyclists --- oxidative stress biomarkers --- antioxidative enzymes --- ultraendurance exercise --- muscle injury --- diet --- reactive oxygen species --- adipose tissue --- antioxidant supplement --- circadian rhythms --- reactive oxygen and nitrogen species (RONS) --- exercise training --- antioxidant --- ApoE --- exercise --- antioxidants --- oxidative stress --- cognition --- motor --- vitamin E --- vitamin C --- aging --- Alzheimer's disease --- lymphocytes --- mitochondrial transmembrane potential decline --- thiobarbituric acid reactive substance --- protein carbonyl --- skeletal muscle --- obesity --- fatigue --- diazoxide --- catalase --- superoxide dismutase --- oxidized glutathione --- reduced glutathione --- hemoglobin --- power output --- eccentric exercise --- redox status --- erythrocyte --- metabolism --- probiotics --- physical exercise --- male cyclists --- oxidative stress biomarkers --- antioxidative enzymes --- ultraendurance exercise --- muscle injury --- diet --- reactive oxygen species --- adipose tissue --- antioxidant supplement --- circadian rhythms --- reactive oxygen and nitrogen species (RONS) --- exercise training --- antioxidant
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Alzheimer’s disease (AD) is an age-related neurological disease that affects tens of millions of people, in addition to their carers. Hallmark features of AD include plaques composed of amyloid beta, as well as neurofibrillary tangles of tau protein. However, despite more than a century of study, the cause of Alzheimer’s disease remains unresolved. The roles of amyloid beta and tau are being questioned and other causes of AD are now under consideration. The contributions of researchers, model organisms, and various hypotheses will be examined in this Special Issue.
HOTAIR --- neurosciences --- sleep disturbance --- positron emission tomography (PET) --- vitamin B complex --- neurodegeneration --- Tau --- miR-15/107 --- default-mode network --- complement receptor 1 --- neuronal differentiation --- epigenetics --- brain glucose metabolism --- oligomerization --- genetic risk --- A?O receptors --- prion --- ryanodine receptor --- type 3 diabetes --- complement --- cognitive behavioral therapy for insomnia --- cognitive function --- epigenome-wide association study --- Alzheimer’s disease --- calcium signaling --- ?-secretase --- tau --- Prolyl isomerases --- NEAT1 --- complement C3b/C4b receptor --- proteostasis --- amyloid beta --- yeast --- slow-wave sleep --- amyloid ? --- nutrition --- 4 --- protein aggregation --- apolipoprotein E --- dementia --- MALAT1 --- inositol 1 --- lncRNAs --- molecular biology --- methylenetetrahydrofolate reductase MTHFR gene --- 5-trisphosphate receptor --- CR1 density --- miR-34c --- aggregation --- heat shock protein --- dendritic spine --- S-adenosylmethionine --- beta amyloid --- ion channel --- inflammation --- sleep fragmentation --- cystathionine-?-lyase CTH gene --- DNA methylation --- heat shock response --- microglia --- drug target discovery --- amyloid-? oligomer --- therapy --- CR1 length polymorphism --- methylome --- APOE gene --- ubiquitin --- magnetic resonance imaging (MRI) --- neuronal degeneration --- type 2 diabetes --- Pin1 --- mild cognitive impairment --- dairy products --- endoplasmic reticulum --- oxidative stress --- Hispanics --- CDK5R1
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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.
Technology: general issues --- Biotechnology --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(-) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages
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Dear colleagues, This Special Issue, “Endothelial Dysfunction: From Pathophysiology to Novel Therapeutic Approaches”, focuses on the pathophysiology of endothelial dysfunction, new biomarkers for endothelial dysfunction related to cardiovascular disorders or tumors, and novel therapeutic approaches for endothelial dysfunctions. Vascular endothelium is an active tissue and plays a crucial role in the maintenance of vascular homeostasis. Chronic exposure to risk factors, such as hypertension, high cholesterolemia, or oxidative stress, induces endothelial dysfunctions and results in a loss of endothelial integrity, smooth muscle cell proliferation, and macrophage recruitment. The pathophysiology of endothelial dysfunction (ED) is complex and multi-factorial factors are involved, such as oxidative stress or chronic inflammation. The primary prevention of cardiovascular risk factors and endothelial dysfunctions, as well as the early detection of or molecular imaging techniques for endothelial dysfunction, helps to prevent the development of cardiovascular disorders. Novel therapeutic approaches or drug delivery systems for endothelial dysfunctions have had promising beneficial effects in preclinical or clinical levels by affecting the progression of atherosclerotic changes, tumor angiogenesis, and host–immune reactions near tumor environments.
Technology: general issues --- Biotechnology --- endothelial cells --- oxidative stress --- inflammageing --- endothelial dysfunction --- aldehyde dehydrogenase-2 --- cardiovascular disease --- neurovascular disease --- vascular inflammation --- APE1/Ref-1 --- cardiovascular diseases --- subcellular localization --- serological biomarkers --- atherosclerosis --- aerobic exercise --- PCSK9 --- LOX-1 --- insulin resistance --- macrophage polarity --- serum γ-glutamyltransferase --- essential hypertension --- cardiovascular risk factors --- angiogenesis --- nargenicin A1 --- compound 9 --- VEGF --- VEGFR2 --- HIF-1α --- electronegative low-density lipoprotein --- LDL(–) --- L5 LDL --- oxidized LDL --- oxLDL --- ADMA --- arginine --- arginine paradox --- BH4 --- blood pressure --- COVID-19 --- dietary supplements --- endothelium --- eNOS uncoupling --- heart failure --- hypertension --- L-arginine --- myocardial infarction --- NADPH --- nitric oxide --- peripheral artery disease --- ApoE knockout mouse --- atorvastatin --- VCAM-1 --- galectin-3 --- neutrophil/lymphocyte ratio --- electronegative LDL --- LDL(−) --- lectin-like oxLDL receptor-1 --- dyslipidemia --- chronic venous insufficiency --- prolyl oligopeptidase (POP) --- inflammation --- endothelial disfunction --- lung disease --- endothelial to mesenchymal transition --- pulmonary hypertension --- pulmonary fibrosis --- metformin --- diabetes --- CV risk --- hyperglycemia --- glycated lipoproteins --- glycated LDL --- glycated HDL --- endothelial cell dysfunction --- molecular mechanisms --- epigenetic factors --- therapeutic approaches --- vasoactive factors --- EndoMT --- TGF-β --- epigenetics --- endothelial cell --- glycolysis --- metabolism --- pathological angiogenesis --- tumor microenvironment --- MRI (magnetic resonance imaging) --- high-fat diets --- plaque burden --- low-level laser therapy --- phototherapy --- vascular disease --- healing --- ischemia --- vascular calcification --- chronic kidney disease --- CKD --- uremic toxins --- hyperphosphatemia --- vascular smooth muscle cells --- VSMCs --- macrophages --- n/a --- LDL(-)
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