Retinoids are a group of vitamin A-related chemicals that are essential to chordate mammals. They regulate a number of basic processes, including embryogenesis and vision. From ingestion to metabolism and the subsequent cellular effects, retinoid levels are tightly regulated in the organism to prevent toxicity. One component of this network, the membrane receptor STRA6, has been shown to be essential in facilitating the cellular entry and exit of retinol. However, recent data suggests that STRA6 may not function merely as a retinoid transporter but also act as a complex signalling hub in its own right, being able to affect cell fate through the integration of retinoid signalling with other key pathways, such as those involving p53, JAK/STAT, Wnt/β catenin and calcium. This may open new therapeutic strategies in diseases like cancer, where these pathways are often compromised. Here, we look at the growing evidence regarding the novel roles of STRA6 beyond its well characterized classic functions.
When a cell is damaged, it must decide how to respond. As a consequence of a variety of stresses, cells can induce well-regulated programmes such as senescence, a persistent proliferative arrest that limits their replication. Alternatively, regulated programmed cell death can be induced to remove the irreversibly damaged cells in a controlled manner. These programmes are mainly triggered and controlled by the tumour suppressor protein p53 and its complex network of effectors, but how it decides between these wildly different responses is not fully understood. This review focuses on the key proteins involved both in the regulation and induction of apoptosis and senescence to examine the key events that determine cell fate following damage. Furthermore, we examine how the regulation and activity of these proteins are altered during the progression of many chronic diseases, including cancer.
There is currently a growing anti-gluten trend which, except for individuals with coeliac disease and non-coeliac gluten sensitivity (NCGS) for whom its intake is contraindicated, results in gluten (the main protein in wheat and other cereals) being considered harmful to health and excluded from diets, largely due to information distributed through social networks. However, in many cases the recommendation to exclude gluten from the diet goes beyond personal choice and is promoted by health professionals. This choice and/or recommendation is especially important to individuals with chronic inflammatory diseases such as rheumatoid arthritis (RA), for which this exclusion is justified to reduce the symptoms of the disease. The aim of this literature review is to assess whether there is scientific evidence to justify the elimination of gluten in patients with RA, neither coeliac nor with NCGS, to improve their symptoms and quality of life. The results of the search on gluten and RA carried out in the Embase database and the extraction of data from 16 articles included in the review are presented. No scientific evidence was found to recommend the exclusion of gluten in patients with RA.
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