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We also reviewed various neurological diseases wherein ER stress/UPR, and autophagy play key roles and also discussed possible pharmacological interventions involving these processes. © 2020 Elsevier Inc. All rights reserved.Virus exploits host cellular machinery to replicate and form new viral progeny and endoplasmic reticulum (ER) plays central role in the interplay between virus and host cell. Here I will discuss how cellular functions of ER being utilized by viruses from different families during different stages of pathogenesis. Flow of knowledge related to this area of research based on interdisciplinary approach, using biochemical and cell biological assays coupled with advanced microscopy strategies, is pushing our understanding of the virus-ER interaction during infection to the next level. © 2020 Elsevier Inc. All rights reserved.The sarco/endoplasmic reticulum is an extensive, dynamic and heterogeneous membranous network that fulfills multiple homeostatic functions. Among them, it compartmentalizes, stores and releases calcium within the intracellular space. In the case of muscle cells, calcium released from the sarco/endoplasmic reticulum in the vicinity of the contractile machinery induces cell contraction. Furthermore, sarco/endoplasmic reticulum-derived calcium also regulates gene transcription in the nucleus, energy metabolism in mitochondria and cytosolic signaling pathways. These diverse and overlapping processes require a highly complex fine-tuning that the sarco/endoplasmic reticulum provides by means of its numerous tubules and cisternae, specialized domains and contacts with other organelles. The sarco/endoplasmic reticulum also possesses a rich calcium-handling machinery, functionally coupled to both contraction-inducing stimuli and the contractile apparatus. Such is the importance of the sarco/endoplasmic reticulum for muscle cell physiology, that alterations in its structure, function or its calcium-handling machinery are intimately associated with the development of cardiometabolic diseases. Cardiac hypertrophy, insulin resistance and arterial hypertension are age-related pathologies with a common mechanism at the muscle cell level the accumulation of damaged proteins at the sarco/endoplasmic reticulum induces a stress response condition termed endoplasmic reticulum stress, which impairs proper organelle function, ultimately leading to pathogenesis. © 2020 Elsevier Inc. All rights reserved.Mitochondria and endoplasmic reticulum (ER) are fundamental in the control of cell physiology regulating several signal transduction pathways. They continuously communicate exchanging messages in their contact sites called MAMs (mitochondria-associated membranes). MAMs are specific microdomains acting as a platform for the sorting of vital and dangerous signals. In recent years increasing evidence reported that multiple scaffold proteins and regulatory factors localize to this subcellular fraction suggesting MAMs as hotspot signaling domains. In this review we describe the current knowledge about MAMs' dynamics and processes, which provided new correlations between MAMs' dysfunctions and human diseases. In fact, MAMs machinery is strictly connected with several pathologies, like neurodegeneration, diabetes and mainly cancer. These pathological events are characterized by alterations in the normal communication between ER and mitochondria, leading to deep metabolic defects that contribute to the progression of the diseases. © 2020 Elsevier Inc. All rights reserved.Several pathological and inflammatory disorders induce a cytoprotective endoplasmic reticulum (ER) stress that aims at reestablishing tissue homeostasis, yet can also ignite lethal signaling pathways leading to apoptotic cell death when ER stress endures. Cells that undergo episodes of ER stress in response to pathological malfunction or cytotoxic agents can expose and release immunomodulatory damaged-associated molecular patterns (DAMPs) on their surface and into the extracellular space, respectively. Immunosuppressive DAMPs inhibit the transfer of antigens from stressed cells to antigen-presenting cells (APCs), whereas immunostimulatory DAMPs can act on APCs to facilitate antigen uptake, processing and presentation to stimulate T cell-mediated adaptive immune responses. Barasertib nmr In this review, we focus on immunomodulatory DAMPs that are released/exposed in conditions of ER stress induced in the context of chronic pathologies and anticancer therapies. © 2020 Elsevier Inc. All rights reserved.Recognizing the contribution art has had in the Mayo Clinic environment since the original Mayo Clinic Building was finished in 1914, Mayo Clinic Proceedings features some of the numerous works of art displayed throughout the buildings and grounds on Mayo Clinic campuses as interpreted by the author. While the global prevalence of both type 1 and type 2 diabetes mellitus is similar in men and women, the consequences of diabetes on associated end-organ complications, including diabetic kidney disease appear to be more sex-specific. Particularly, women with diabetes have higher mortality rates for diabetes-related deaths, and higher prevalence of diabetic kidney disease risk factors such as hypertension, hyperglycemia, obesity, and dyslipidemia. However, the evidence for the impact of sex on diabetic kidney disease prevalence and disease progression is limited and inconsistent. Although most studies agree that the protective effect of the female sex against the development of kidney disease is diminished in the setting of diabetes, the reasons for this observation are unclear. Whether or not sex differences exist in the risk of diabetic kidney disease is also unclear, with studies reporting either higher risk in men, women, or no sex differences. Despite the remaining controversies, some of the factors that associate with sex differences in the risk of diabetic kidney disease are age at onset, and type and duration of diabetes. There is growing appreciation of the importance of sex hormones in the regulation of renal function, with estrogens generally considered to be renoprotective. Although some progress has been made towards better understanding of the mechanisms by which sex hormones play a role in the pathophysiology of diabetic kidney disease, the translational potential of this knowledge is still underappreciated. A better understanding of sex differences in diabetic kidney disease may provide basis for personalized and sex-specific treatment of diabetic kidney disease. Published by Elsevier Inc.

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