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Reinke H.,Heinrich Heine University Dusseldorf | Reinke H.,IUF Leibniz Research Institute for Environmental Medicine | Asher G.,Weizmann Institute of Science
Gastroenterology | Year: 2016

The circadian clock is an endogenous biological timekeeping system that synchronizes physiology and behavior to day/night cycles. A wide variety of processes throughout the entire gastrointestinal tract and notably the liver appear to be under circadian control. These include various metabolic functions such as nutrient uptake, processing, and detoxification, which align organ function to cycle with nutrient supply and demand. Remarkably, genetic or environmental disruption of the circadian clock can cause metabolic diseases or exacerbate pathological states. In addition, modern lifestyles force more and more people worldwide into asynchrony between the external time and their circadian clock, resulting in a constant state of social jetlag. Recent evidence indicates that interactions between altered energy metabolism and disruptions in the circadian clock create a downward spiral that can lead to diabetes and other metabolic diseases. In this review, we provide an overview of rhythmic processes in the liver and highlight the functions of circadian clock genes under physiological and pathological conditions; we focus on their roles in regulation of hepatic glucose as well as lipid and bile acid metabolism and detoxification and their potential effects on the development of fatty liver and nonalcoholic steatohepatitis. © 2016 AGA Institute. Source


Shao D.,Rutgers University | Oka S.-I.,Rutgers University | Brady C.D.,Rutgers University | Haendeler J.,IUF Leibniz Research Institute for Environmental Medicine | And 2 more authors.
Journal of Molecular and Cellular Cardiology | Year: 2012

Oxidative stress is presumed to be involved in the pathogenesis of many diseases, including cardiovascular disease. However, oxidants are also generated in healthy cells, and increasing evidence suggests that they can act as signaling molecules. The intracellular reduction-oxidation (redox) status is tightly regulated by oxidant and antioxidant systems. Imbalance between them causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, leading to dysregulation. In this review, we will briefly summarize the aspects of ROS generation and neutralization mechanisms in the cardiovascular system. ROS can regulate cell signaling through oxidation and reduction of specific amino acids within proteins. Structural changes during post-translational modification allow modification of protein activity which can result in altered cellular function. We will focus on the molecular basis of redox protein modification and how this regulatory mechanism affects signal transduction in the cardiovascular system. Finally, we will discuss some techniques applied to monitoring redox status and identifying redox-sensitive proteins in the heart. This article is part of a Special Section entitled "Post-translational Modification.". © 2011 Elsevier Ltd. Source


Krutmann J.,IUF Leibniz Research Institute for Environmental Medicine | Morita A.,Nagoya City University | Chung J.H.,Seoul National University
Journal of Investigative Dermatology | Year: 2012

The health consequences of sun exposure have concerned mankind for more than 100 years. Recent molecular studies in photodermatology have greatly advanced our understanding of this important topic. We will illustrate this progress by focusing on the following selected topics: (i) the nature of the DNA damage-independent part of the UVB response of human skin and the role of the arylhydrocarbon receptor in cutaneous biology, (ii) the contribution of wavelengths beyond the UV spectrum to solar radiation-induced skin damage, (iii) the emerging evidence that subcutaneous fat is a target tissue for sunlight, and (iv) the most recent insight into the mode of action of phototherapy. © 2012 The Society for Investigative Dermatology. Source


Schiavi A.,IUF Leibniz Research Institute for Environmental Medicine | Schiavi A.,University of Rome Tor Vergata | Ventura N.,Heinrich Heine University Dusseldorf | Ventura N.,IUF Leibniz Research Institute for Environmental Medicine | Ventura N.,University of Rome Tor Vergata
Experimental Gerontology | Year: 2014

Mitochondria are highly dynamic organelles which play a central role in cellular homeostasis. Mitochondrial dysfunction leads to life-threatening disorders and accelerates the aging process. Surprisingly, on the other hand, a mild reduction of mitochondria functionality can have pro-longevity effects in organisms spanning from yeast to mammals. Autophagy is a fundamental cellular housekeeping process that needs to be finely regulated for proper cell and organism survival, as underlined by the fact that both its over- and its defective activation have been associated with diseases and accelerated aging. A reciprocal interplay exists between mitochondria and autophagy, which is needed to constantly adjust cellular energy metabolism in different pathophysiological conditions. Here we review general features of mitochondrial function and autophagy with particular focus on their crosstalk and its possible implication in the aging process. © 2014 Elsevier Inc. Source


Haarmann-Stemmann T.,IUF Leibniz Research Institute for Environmental Medicine | Esser C.,IUF Leibniz Research Institute for Environmental Medicine | Krutmann J.,IUF Leibniz Research Institute for Environmental Medicine | Krutmann J.,Heinrich Heine University Dusseldorf
Journal of Investigative Dermatology | Year: 2015

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor expressed in all skin cell types, which is critically involved in the pathogenesis of a variety of skin diseases and thus represents a potential therapeutic target. Recent studies indicate that blocking AHR activation is desirable in some skin conditions, whereas the opposite, i.e., stimulation of AHR activation, is beneficial in another group of skin disorders. We here propose a model based on qualitative differences in canonical versus non-canonical AHR signaling to reconcile these seemingly contradictory observations. © 2015 The Society for Investigative Dermatology. Source

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