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      Autofagia un sistema celular de limpieza clave para la salud. Una visita al Premio Nobel de Fisiología o Medicina de 2016 Translated title: Autophagy, a key cellular cleansing system for health. A visit to the 2016 Nobel Prize in Physiology or Medicine

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          Abstract

          Resumen Introducción. En 2016, el Instituto Karolinska premió a Yoshinori Ohsumi con el Premio Nobel de Fisiología y Medicina por sus estudios en autofagia. Posteriormente muchas investigaciones han demostrado la importancia de este proceso en la salud. Métodos. Se revisan tres aspectos: a) la información del Comité del Nobel sobre las investigaciones del galardonado; b) los mecanismos moleculares implicados en la autofagia; y c) la relación entre autofagia y salud. Resultados. Se presentan los aspectos más relevantes de la investigación sobre la autofagia, desde las investigaciones de De Duve con los lisosomas hasta algunos detalles moleculares relevantes. Se comentan datos biográficos de Ohsumi y aspectos de su investigación que llevaron al Nobel; también las características de los tres tipos de autofagia: macrofagia, microfagia y dependiente de chaperonas. Este proceso es altamente dependiente del estado nutricional, del estrés y de la expresión de ciertos genes, particularmente los de autofagia (ATG). Alteraciones en la expresión o la existencia de polimorfismos en ATG originan cambios significativos en la formación de los autofagosomas. Se explica la importancia en la salud y algunas patologías muy prevalentes del reciclado de células completas y de sus componentes aislados, así como el papel de la interacción de algunos fármacos en la función autofágica. Conclusión. La autofagia es un proceso celular muy común, altamente dependiente del estado nutricional y de la expresión y polimorfismos de los ATG. Es determinante en la maduración, desarrollo y salud, y participa de forma relevante en el envejecimiento y en la prevención de enfermedades degenerativas.

          Translated abstract

          Abstract Introduction. In 2016, the Karolinska Institute awarded Yoshinori Ohsumi the Nobel Prize in Physiology and Medicine for his studies on autophagy. Subsequently, many investigations have demonstrated the role of this process in health. Methods. Three aspects are reviewed: a) the information given by the Nobel Committee on the laureate's research; b) the molecular mechanisms involved in autophagy; and c) the relationship between autophagy and health. Results. The most relevant aspects of autophagy research are presented, from De Duve's research with lysosomes to some relevant molecular details. Ohsumi's biographical data and aspects of his research that led to the Nobel are discussed; also, the characteristics of the three types of autophagy: macrophagy, microphagy and chaperone-dependent. Autophagy is highly dependent on nutritional status, stress, and the expression of certain genes, particularly the so-called autophagy-related genes (ATG). Alterations in the expression or the existence of polymorphisms in ATG cause significant changes in the formation of autophagosomes. The importance in health and some very prevalent pathologies of the recycling of whole cells and their isolated components is explained, as well as the role of the interaction of some drugs in the autophagic function. Conclusion: Autophagy is a very common cellular process, highly dependent on nutritional status and ATG expression and polymorphisms. It is determinant in maturation, development, and health, and participates in a relevant way in aging and in the prevention of degenerative diseases.

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          Autophagy regulates lipid metabolism.

          The intracellular storage and utilization of lipids are critical to maintain cellular energy homeostasis. During nutrient deprivation, cellular lipids stored as triglycerides in lipid droplets are hydrolysed into fatty acids for energy. A second cellular response to starvation is the induction of autophagy, which delivers intracellular proteins and organelles sequestered in double-membrane vesicles (autophagosomes) to lysosomes for degradation and use as an energy source. Lipolysis and autophagy share similarities in regulation and function but are not known to be interrelated. Here we show a previously unknown function for autophagy in regulating intracellular lipid stores (macrolipophagy). Lipid droplets and autophagic components associated during nutrient deprivation, and inhibition of autophagy in cultured hepatocytes and mouse liver increased triglyceride storage in lipid droplets. This study identifies a critical function for autophagy in lipid metabolism that could have important implications for human diseases with lipid over-accumulation such as those that comprise the metabolic syndrome.
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            The machinery of macroautophagy.

            Autophagy is a primarily degradative pathway that takes place in all eukaryotic cells. It is used for recycling cytoplasm to generate macromolecular building blocks and energy under stress conditions, to remove superfluous and damaged organelles to adapt to changing nutrient conditions and to maintain cellular homeostasis. In addition, autophagy plays a critical role in cytoprotection by preventing the accumulation of toxic proteins and through its action in various aspects of immunity including the elimination of invasive microbes and its participation in antigen presentation. The most prevalent form of autophagy is macroautophagy, and during this process, the cell forms a double-membrane sequestering compartment termed the phagophore, which matures into an autophagosome. Following delivery to the vacuole or lysosome, the cargo is degraded and the resulting macromolecules are released back into the cytosol for reuse. The past two decades have resulted in a tremendous increase with regard to the molecular studies of autophagy being carried out in yeast and other eukaryotes. Part of the surge in interest in this topic is due to the connection of autophagy with a wide range of human pathophysiologies including cancer, myopathies, diabetes and neurodegenerative disease. However, there are still many aspects of autophagy that remain unclear, including the process of phagophore formation, the regulatory mechanisms that control its induction and the function of most of the autophagy-related proteins. In this review, we focus on macroautophagy, briefly describing the discovery of this process in mammalian cells, discussing the current views concerning the donor membrane that forms the phagophore, and characterizing the autophagy machinery including the available structural information.
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              The coming of age of chaperone-mediated autophagy

              Chaperone-mediated autophagy (CMA) was the first studied process that indicated that degradation of intracellular components by the lysosome can be selective — a concept that is now well accepted for other forms of autophagy. Lysosomes can degrade cellular cytosol in a nonspecific manner but can also discriminate what to target for degradation with the involvement of a degradation tag, a chaperone and a sophisticated mechanism to make the selected proteins cross the lysosomal membrane through a dedicated translocation complex. Recent studies modulating CMA activity in vivo using transgenic mouse models have demonstrated that selectivity confers on CMA the ability to participate in the regulation of multiple cellular functions. Timely degradation of specific cellular proteins by CMA modulates, for example, glucose and lipid metabolism, DNA repair, cellular reprograming and the cellular response to stress. These findings expand the physiological relevance of CMA beyond its originally identified role in protein quality control and reveal that CMA failure with age may aggravate diseases, such as ageing-associated neurodegeneration and cancer.
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                Author and article information

                Journal
                jonnpr
                Journal of Negative and No Positive Results
                JONNPR
                Research and Science S.L. (Madrid, Madrid, Spain )
                2529-850X
                March 2023
                : 8
                : 1
                : 417-439
                Affiliations
                [2] Madrid orgnameUniversidad Complutense de Madrid orgdiv1Facultad de Farmacia Spain
                [1] New York orgnameAlbert Einstein College of Medicine orgdiv1Facultad de Farmacia United States
                Article
                S2529-850X2023000100001 S2529-850X(23)00800100001
                10.19230/jonnpr.4912
                4a454e06-cbe2-4747-9216-257a673d28e1

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 07 October 2022
                : 24 November 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 61, Pages: 23
                Product

                SciELO Spain

                Categories
                Revisión

                macrophagia,Autophagy,Nobel Prize,microphagia,chaperones,health,diseases,Autofagia,Premio Nobel,macrofagia,microfagia,chaperonas,salud,enfermedades

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