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The purpose of this Special Issue “The Role of Nutrition in Cardiometabolic Health: Experimental, Clinical, and Community-Based Evidence” is to publish a focused, coherent, impactful, and well-cited volume on how nutrition influences diverse cardiometabolic risk factors. Cardiometabolic diseases, such as coronary heart disease, stroke, type 2 diabetes mellitus, and obesity, is the leading cause of death worldwide. In recent years, dietary habits have shifted all over the globe. At the same time, a constantly growing body of evidence demonstrates the role of caloric intake and dietary composition as determinants of cardiometabolic health. Suboptimal diet predisposes to a myriad of cardiometabolic risk factors such as impaired glucose metabolism, insulin resistance, dyslipidaemias, and high blood pressure.

Medicine --- vitamin D --- obesity --- microvascular --- bariatric surgery --- weight loss --- nitric oxide --- cardiac remodeling --- cardiac dysfunction --- echocardiogram --- obese rats --- high-fat high-sugar diet --- vascular stiffness --- blood pressure --- whey protein isolate --- older adults --- dietary factor --- cardiovascular disease --- umbrella review --- low-carbohydrate diet --- hypocaloric --- isocaloric --- women health --- conduit artery --- microvasculature --- cardiovascular risks --- primary prevention --- homocysteine --- folate --- vitamin B12 --- vascular dysfunction --- hepatocyte --- TGR5 --- glucose regulation --- homocysteine and vascular disease --- H3K27me3 --- epigenetics --- atherosclerosis --- MRI (magnetic resonance imaging) --- liver --- metabolic regulation --- laparoscopic sleeve gastrectomy --- micronutrients --- deficiency --- body mass index --- cardiotonic steroids --- left ventricular mass --- marinobufagenin --- dietary salt intake --- young adults

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Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

Medicine --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage

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The natriuretic peptides (NPs) family includes a class of hormones and their receptors needed for the physiological control of cardiovascular functions. The discovery of NPs provided a fundamental contribution into our understanding of the physiological regulation of blood pressure, and of heart and kidney functions. NPs have also been implicated in the pathogenesis of several cardiovascular diseases (CVDs), including hypertension, atherosclerosis, heart failure, and stroke. A fine comprehension of the molecular mechanisms dependent from NPs and underlying the promotion of cardiovascular damage has contributed to improve our understanding of the molecular basis of all major CVDs. Finally, the opportunity to target NPs in order to develop new therapeutic tools for a better treatment of CVDs has been developed over the years. The current Special Issue of the Journal covers all major aspects of the molecular implications of NPs in physiology and pathology of the cardiovascular system, including NP-based therapeutic approaches.

postmortem biochemistry --- medulla --- animal models --- remodeling --- BNP --- PCSK9 --- guanylyl cyclase/natriuretic peptide receptor-A --- cardiorenal syndrome --- forensic medicine --- preserved ejection fraction --- kidney --- renin-angiotensin-aldosterone system --- atrial fibrillation --- vasopressor --- congestive heart failure --- atrial natriuretic peptide --- gene-knockout --- obesity --- heart failure --- angiogenesis --- adipose tissue --- vascular --- LDL receptor --- metabolic syndrome --- linkage analysis --- cardiometabolic disease --- cardiomyocyte --- cardiac dysfunction --- cardiac hypertrophy --- insulin --- lipid metabolism --- cGMP --- Idiopathic Pulmonary Arterial Hypertension (IPAH) --- Natriuretic Peptide Clearance Receptor (NPR-C) signaling --- gene-duplication --- renin–angiotensin system --- natriuretic peptides --- angiotensin receptor–neprilysin inhibitor --- cardiac remodelling --- ARNi --- NT-proBNP --- inflammation --- pulmonary arterial hypertension --- vascular homeostasis --- endothelial cell --- Atrial Natriuretic peptide --- natriuretic peptide --- vasodilator --- stroke --- genetic variants --- arterial hypertension --- fibroblast --- MANP --- hypertension --- guanylyl cyclase receptor A

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This book “Oxidative Stress Modulators and Functional Foods” is focused on the antioxidant role of natural products, involving their ability to modulate oxidative stress and/or reverse disease studied both in vitro and in animal models. Additionally, the molecular mechanisms of these actions and the modulation of signalling pathways related to inflammation, apoptosis, and survival response in the redox system by natural products are included.

Medicine --- Pharmaceutical industries --- high sugar-fat diet --- obesity --- β-adrenergic system --- cardiac dysfunction --- lycopene --- tomato-oleoresin --- coumarin --- pteryxin --- HO-1 --- Nrf2 --- oxidative stress --- Peucedanum japonicum Thunb --- RAW264.7 cells --- polysaccharide --- jujube pomace --- structural analysis --- antioxidant activity --- epigallocatechin-gallate --- liposomes --- diabetes mellitus --- antioxidant --- dendrimer --- electronic effect --- hydrogen atom transfer (HAT) --- single electron transfer-proton transfer (SET-PT) --- sequential proton loss electron transfer (SPLET) --- DPPH --- ultraviolet B --- gradient ethanol precipitation --- fucoidan --- HaCaT keratinocyte --- heme oxygenase-1 --- nutricosmetic --- folic acid --- nitric oxide --- neural tube defects --- NOR3 --- ESR --- LC/MS --- Benzo[a]pyrene --- myricetin --- BPDE-DNA adduct --- phase detoxifying enzyme --- Quamoclit angulata --- type 2 diabetes --- kidney damage --- inflammation --- apoptosis --- fibrosis --- Sargassum horneri --- (–)-loliolide --- fine dust --- HaCaT --- bilberry --- lingonberry --- polyphenols --- antioxidant compounds --- antimicrobial activity --- antimutagenicity --- altitude variations --- mitochondria --- neurodegeneration --- nutrient --- QM-ORSA --- antioxidative mechanisms --- reaction rate constants --- physiological conditions --- zebrafish embryo --- in vivo model --- antioxidant effect --- cudratrixanthone O --- reactive oxygen species --- nuclear transcription factor erythroid-2-like factor 2 --- hemeoxygenase-1 --- n/a --- (-)-loliolide

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Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn’s disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- n/a --- Crohn's disease