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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Science: general issues --- Physiology --- thermogenesis --- mitochondria --- uncoupling proteins (UCPs) --- obesity --- metabolic disease --- adipocytes --- dietary components

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Alteration in adequate energy balance maintenance results in serious disturbances such as obesity and its related metabolic disorders. In Mammals, energy balance is homeostatically controlled through hormonal and neuroendocrine systems which cooperation is based on cross-talk between central and peripheral signals. The hypothalamus as well as peripheral hormones among which adipokines from adipose tissue and thyroid hormones play a crucial role in energy homeostasis. Unraveling the physiological, cellular and molecular mechanisms through which hormonal and neuroendocrine systems regulate energy balance has been a long-standing challenge in biology and is now more necessary when considering the world-wide increasing prevalence of obesity. Indeed, recognizing and understanding the biochemical and nutrient signaling pathways contributing to the nervous and endocrine integration of physiological mechanisms involved in the normal and/or abnormal regulation of energy balance is fundamental also to the development of new, effective, and targeted treatments for obesity. Recent studies have highlighted the role of hypothalamic pro-opiomelanocortin-expressing neurons in the regulation of energy homeostasis by controlling energy expenditure and food intake. This is accomplished through a precise balance of production and degradation of a-melanocyte-stimulating hormone, an anorexigenic neuropeptide which is degraded to an inactive form unable to inhibit food intake by the key enzyme prolyl carboxypeptidase (PRCP), thus suggesting that pharmacologic approaches targeting PRCP may provide a novel and effective option for the management of obesity and its associated metabolic disorders. Indeed, efforts have been made to generate potent, brain-penetrant PRCP inhibitors. Weight loss due to negative energy balance is a goal for obese subjects not always reachable by dietary caloric restriction or increased physical activity. Lipid-lowering therapies have been suggested to have potential benefits, however, the establishment of comprehensive therapeutic strategies is still awaited. Recently, it has been reported that thyroid hormone (TH)- derivatives such as 3,5-diiodothyronine and 3-iodothyronamine possess interesting biological activities, opening new perspectives in thyroid physiology and TH derivatives therapeutic usage. Moreover, several studies, focusing on the interaction between thyroid hormone (TH), the autonomic nervous system and the liver, revealed an important role for the hypothalamus in the differential effects of TH on autonomic outflow to peripheral organs controlling energy balance. This Research Topic aims to give a comprehensive and integrate view of the factors involved in the endocrine and neuroendocrine signaling in energy balance regulation to highlight their involvement into physiological processes and regulatory systems as well as their perturbation during pathological processes.

Uncoupling --- Mitochondria --- catch up fat --- brown adipose tissue --- Thyroid Hormones --- Lipid Metabolism --- energy balance --- Apelin --- melanocortin --- Adipogenesis

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Kidney disease is a complex health problem, often coinciding with cardiovascular pathology (e.g. hypertension) and metabolic disturbances (e.g. obesity and diabetes). It is also a disturbingly fast growing global public health problem, e.g. chronic kidney disease affects an estimated ~9-16% of the population. Besides the public health issues this results in a large economic burden as kidney diseases contributes disproportionally to about a quarter of total health care costs. Experimental and clinical data solidly support the view that kidney tissue hypoxia plays a critical and intricate role during the genesis and progression of both chronic and acute kidney diseases. This research field is currently at the very beginning of integrating pre-clinical with clinical research in which hypoxia related mechanism are quantified by non-invasive imaging. In combination with the fact that some key questions remain unanswered, this offers exciting new research perspectives that are waiting to be explored. With this Research Topic we aim to discuss and find answers to the following research question: 1) What are the temporal relationships between hypoxia and kidney disease? 2) Can we demonstration causation between hypoxia and kidney disease? 3) Can renal hypoxia be considered as a treatment target in kidney disease? 4) Can hypoxia (e.g. in the urine) be considered a biomarker of kidney disease? 5) Does hypoxia ramp-up sympathetic activity? 6) Does hypoxia trigger inflammation? 7) Is hypoxia caused by changes in sodium reabsorption and/or mitochondrial function? 8) Which molecular mechanisms are involved in hypoxia in kidney disease? 9) Which gene expressions change due to hypoxia in kidney disease? 10) Can we generate new and translational insights using non-invasive imaging technologies? Our overall aim is identify the mediators/controllers of hypoxia in kidney disease. If we understand more about the sequence of events leading to hypoxia, its regulation and consequences in renal disease, we might be able to have a major impact in clinical practice. I.e. more accurate and earlier diagnosis, novel treatment targets, and novel therapies.

chronic kidney disease --- magnetic resonance imaging --- kidney transplantation --- idney hypoxia --- sympathetic nerve activity --- mitochondrial uncoupling --- telemetry --- hypertension

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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.

Medicine --- Pharmacology --- diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a

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The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.

diabetic kidney disease --- caloric restriction --- NADH/NAD+ --- redox imbalance --- mitochondrial homeostasis --- mitophagy --- oxidative stress --- kidney allograft --- kidney rejection --- ischemia --- acute kidney injury (AKI) --- chronic kidney disease (CKD) --- tricarboxylic acid (TCA) cycle --- mitochondrial metabolism --- mitochondrial redox signaling --- mitochondrial proteins --- oxidative phosphorylation (OXPHOS) --- fatty acid (FA) β-oxidation --- mitochondrial dynamics --- biogenesis --- diabetes --- kidney --- mitochondria --- Oryza sativa --- rice husk --- TCA cycle metabolites --- kidney diseases --- renalase --- chronic kidney disease --- major adverse cardiovascular outcomes --- cadmium --- kidney injury --- renal toxicity --- oxidative damage --- proximal tubule --- controlled oxygenated rewarming --- mitochondrial uncoupling --- rewarming injury --- temperature paradox --- redox --- mitochondrial dysfunction --- SGLT2 --- mitochondrial reactive oxygen species --- Warburg effect --- podocytopathies --- mitochondrial oxidative stress --- reactive oxygen species (ROS) --- antioxidant defense --- cell death --- n/a