Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.

Antioxidants --- Metabolomics --- Stroke --- Exercise --- ischemia/reperfusion injury --- mitochondria and chaperones --- Pulmonary hypertention --- reactive oxygen and nitrogen species --- cardiac preconditioning and postconditioning --- Endothelium

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The role of ROS/RNS signaling in cardiovascular functions and diseases is increasingly emerging in the last decades. The involvement of ROS/RNS in the control of a large number of cardiovascular functions like the regulation of the vascular tone, the control of blood pressure or myocyte excitation-contraction coupling and force development has been broadly investigated and in part clarified. On the other hand, many efforts have been focused in clarifying the redox mechanisms involved in cardiovascular diseases like ischemia/reperfusion injury, diabetes-associated cardiovascular dysfunctions, atherosclerosis or hypertension, just to mention the major ones. However, in most cases the two levels of investigation remain separate and not interlaced, failing in the attempt to provide a unified vision of the pathophysiologic mechanisms of cardiovascular diseases. The major aim of the Research Topic has been to collect original papers and review articles dealing with the issue from basic to translation research point of views. The topic includes contributions that highlight different interesting aspects of cardiovascular biology with an integrated approach useful for the development of new ideas and advancements in the field of redox signaling in the control of normal cardiovascular functions and their disruption in diseases.

Antioxidants --- Metabolomics --- Stroke --- Exercise --- ischemia/reperfusion injury --- mitochondria and chaperones --- Pulmonary hypertention --- reactive oxygen and nitrogen species --- cardiac preconditioning and postconditioning --- Endothelium

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The book “Protective and Detrimental Role of Heme Oxygenase-1”, includes a selection of original research papers and reviews aimed at understanding the dual role (protective and detrimental) of HO-1 and the involved signaling pathways. Original research papers and reviews aimed at the identification of natural molecules or new synthetic compounds able to modulate HO-1 activity/expression help make HO-1 a potential therapeutic target for the amelioration of various diseases.

coronary artery disease --- n/a --- glucocorticoid receptor --- antigen presentation --- analgesia --- chemotherapy --- locus coeruleus --- Sirtuin 1 --- thiol groups --- Heme Oxygenase-1 --- Betula etnensis Raf. --- heme oxygenase 1 --- tolerance --- heme oxygenase --- atherosclerosis --- nitric oxide --- caloric restriction --- liver --- carbon monoxide --- ER stress --- heme oxygenase-1 --- mineralocorticoid receptor --- Type 1 diabetes mellitus (T1D) --- Gamma-Glutamyl-Cysteine Ligase (GGCL) --- angiotensin II --- bilirubin --- Heme oxygenase-1 (HO-1) inducers --- Inducible nitric oxide synthase (iNOS) --- HO-1 activity inhibitor --- ferroptosis --- Myristica fragrans kernels --- glutathione --- high-pressure gas --- apoptosis --- HO-1 --- diabetes mellitus --- Caffeic acid phenethyl ester (CAPE) --- carotid plaque --- ischemia–reperfusion injury --- ANTIGEN presenting cell --- LPS --- endoplasmic reticulum stress --- hemoglobin --- Pancreatic oxidative damage --- Colon cancer --- inflammation --- reactive oxygen species --- inflammatory pain --- paracetamol --- cardiomyopathy --- heme oxigenase-1 --- adipocytes --- sirtuin 1 --- peripheral artery disease --- PGC-1? --- heme --- Reactive oxygen species (ROS) --- metformin --- GR --- prostate cancer --- NF-?B --- hyperbilirubinemia --- iron --- Tet-ON system --- lung preservation --- oxidative stress --- Gunn rats --- Dimethylarginine dimethylaminohydrolase-1 (DDAH-1) --- ischemia-reperfusion injury

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Coronary heart disease. --- Calcium --- Coronary Disease --- Vascular Calcification. --- Calcium. --- Plaque, Atherosclerotic. --- Physiological effect. --- diagnostic imaging. --- therapy. --- Atheroma --- Atheromatous Plaques --- Atherosclerotic Plaque --- Atherosclerotic Plaques --- Fatty Streak, Arterial --- Fibroatheroma --- Fibroatheromatous Plaques --- Atheromatous Plaque --- Arterial Fatty Streak --- Arterial Fatty Streaks --- Atheromas --- Fibroatheromas --- Fibroatheromatous Plaque --- Plaque, Atheromatous --- Plaque, Fibroatheromatous --- Streak, Arterial Fatty --- Atherosclerosis --- Blood Coagulation Factor IV --- Calcium-40 --- Coagulation Factor IV --- Factor IV --- Calcium 40 --- Factor IV, Coagulation --- Vascular Calcinosis --- Calcification, Vascular --- Calcinosis, Vascular --- Vascular Calcifications --- Vascular Calcinoses --- Vascular Stiffness --- Coronary arteries --- Coronary arteriosclerosis --- Coronary disease --- Coronary thrombosis --- Ischemic heart disease --- Myocardial ischemia --- Heart --- Type A behavior --- Diseases

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The plant-derived polyphenol curcumin has been used in promoting health and combating disease for thousands of years. Its therapeutic effects have been successfully utilized in Ayurvedic and Traditional Chinese Medicine in order to treat inflammatory diseases. Current results from modern biomolecular research reveal the modulatory effects of curcumin on a variety of signal transduction pathways associated with inflammation and cancer. In this context, curcumin’s antioxidant, anti-inflammatory, anti-tumorigenic, and even anti-metastatic activities are discussed. On the cellular level, the reduced activity of several transcription factors (such as NFkB or AP-1) and the suppression of inflammatory cytokines, matrix degrading enzymes, metastasis related genes and even microRNAs are reported. On functional levels, these molecular effects translate into reduced proliferative, invasive, and metastatic capacity, as well as induced tumor cell apoptosis. All these effects have been observed not only in vitro but also in animal models. In combination with anti-neoplastic drugs like Taxol, kinase inhibitors, and radiation therapy, curcumin potentiates the drugs’ therapeutic power and can protect against undesired side effects. Natural plant-derived compounds like curcumin have one significant advantage: They do not usually cause side effects. This feature qualifies curcumin for primary prevention in healthy persons with a predisposition to cancer, arteriosclerosis, or chronic inflammatory diseases. Nonetheless, curcumin is considered safe, although potential toxic effects stemming from high dosages, long-term intake, and pharmacological interactions with other compounds have yet to be assessed. This Special Issue examines in detail and updates current research on the molecular targets, protective effects, and modes of action of natural plant-derived compounds and their roles in the prevention and treatment of human diseases.

minerals --- cancer treatment --- chitosan --- n/a --- neurodegeneration --- antioxidant activity --- senescence --- tumor proliferation --- nanoparticles --- antimicrobial agents --- oxidative metabolites --- drug discovery --- Akt/mTOR signaling --- micronutrients --- ulcerative colitis --- transmission electron microscopy --- metabolic reprogramming --- curcumin --- death receptor --- chaperone-mediated autophagy --- wound healing --- brain ischemia --- autophagy --- Alzheimer’s disease --- genes --- transthyretin --- inflammatory bowel disease --- cellular pathway --- centrifugal partition chromatography --- nutrition --- amyloid --- Curcuma longa --- protein aggregation --- supportive care --- IL-17 --- senolytics --- complementary medicine --- macronutrients --- structure activity relationship --- gastroprotection --- Zingiberaceae --- anti-inflamation --- TLC bioautography --- microbiota --- glioblastoma multiforme --- amyloidosis --- SHMT2 --- antioxidants --- silica --- apoptosis --- reflux esophagitis --- gastric ulcer --- TLC-MS --- anti-cancer --- anticancer --- ImageJ --- anti-tumor --- delivery system --- wound --- Helicobacter pylori --- direct protein binding --- protein misfolding --- tumor growth --- diet --- Crohn’s disease --- hydrostatic counter-current chromatography --- ageing --- renal cell cancer --- gastric cancer --- amino-acids --- STAT3 --- mechanism of action --- inflamm-aging --- mitophagy --- necrotizing enterocolitis --- cell cycling --- vitamins --- turmeric tuber --- cancer --- tau protein --- Alzheimer's disease --- Crohn's disease