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      Megestrol acetate improves cardiac function in a model of cancer cachexia-induced cardiomyopathy by autophagic modulation.

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          Abstract

          Cachexia is a complex metabolic syndrome associated with cancer. One of the features of cachexia is the loss of muscle mass, characterized by an imbalance between protein synthesis and protein degradation. Muscle atrophy is caused by the hyperactivation of some of the main cellular catabolic pathways, including autophagy. Cachexia also affects the cardiac muscle. As a consequence of the atrophy of the heart, cardiac function is impaired and mortality is increased. Anti-cachectic therapy in patients with cancer cachexia is so far limited to nutritional support and anabolic steroids. The use of the appetite stimulant megestrol acetate (MA) has been discussed as a treatment for cachexia.

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          Most cited references48

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          TRAF6 is a signal transducer for interleukin-1.

          Z. Cao, J Xiong, M Takeuchi … (1996)
          Many cytokines signal through different cell-surface receptors to activate the transcription factor NF-kappaB. Members of the TRAF protein family have been implicated in the activation of NF-kappaB by the tumour-necrosis factor (TNF)-receptor superfamily. Here we report the identification of a new TRAF family member, designated TRAF6. When overexpressed in human 293 cells, TRAF6 activates NF-kappaB. A dominant-negative mutant of TRAF6 inhibits NF-kappaB activation signalled by interleukin-1 (IL-1) but not by TNF. IL-1 treatment of 293 cells induces the association of TRAF6 with IRAK, a serine/threonine kinase that is rapidly recruited to the IL-1 receptor after IL-1 induction. These findings indicate that TRAF proteins may function as signal transducers for distinct receptor families and that TRAF6 participates in IL-1 signalling.
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            The Role of the Selective Adaptor p62 and Ubiquitin-Like Proteins in Autophagy

            Mónika Lippai, Péter Löw (2014)
            The ubiquitin-proteasome system and autophagy were long viewed as independent, parallel degradation systems with no point of intersection. By now we know that these degradation pathways share certain substrates and regulatory molecules and show coordinated and compensatory function. Two ubiquitin-like protein conjugation pathways were discovered that are required for autophagosome biogenesis: the Atg12-Atg5-Atg16 and Atg8 systems. Autophagy has been considered to be essentially a nonselective process, but it turned out to be at least partially selective. Selective substrates of autophagy include damaged mitochondria, intracellular pathogens, and even a subset of cytosolic proteins with the help of ubiquitin-binding autophagic adaptors, such as p62/SQSTM1, NBR1, NDP52, and Optineurin. These proteins selectively recognize autophagic cargo and mediate its engulfment into autophagosomes by binding to the small ubiquitin-like modifiers that belong to the Atg8/LC3 family.
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              Autophagic degradation contributes to muscle wasting in cancer cachexia.

              Fabio Penna, Domiziana Costamagna, Fabrizio Pin … (2013)
              Muscle protein wasting in cancer cachexia is a critical problem. The underlying mechanisms are still unclear, although the ubiquitin-proteasome system has been involved in the degradation of bulk myofibrillar proteins. The present work has been aimed to investigate whether autophagic degradation also plays a role in the onset of muscle depletion in cancer-bearing animals and in glucocorticoid-induced atrophy and sarcopenia of aging. The results show that autophagy is induced in muscle in three different models of cancer cachexia and in glucocorticoid-treated mice. In contrast, autophagic degradation in the muscle of sarcopenic animals is impaired but can be reactivated by calorie restriction. These results further demonstrate that different mechanisms are involved in pathologic muscle wasting and that autophagy, either excessive or defective, contributes to the complicated network that leads to muscle atrophy. In this regard, particularly intriguing is the observation that in cancer hosts and tumor necrosis factor α-treated C2C12 myotubes, insulin can only partially blunt autophagy induction. This finding suggests that autophagy is triggered through mechanisms that cannot be circumvented by using classic upstream modulators, prompting us to identify more effective approaches to target this proteolytic system. Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J Cachexia Sarcopenia Muscle
                Title: Journal of cachexia, sarcopenia and muscle
                Publisher: Wiley-Blackwell
                ISSN (Electronic): 2190-6009
                ISSN (Print): 2190-5991
                Publication date (Electronic): Dec 2016
                Volume: 7
                Issue: 5
                Affiliations
                [1 ] Institute of Research for Food Safety and Health (IRC-FSH) University of Catanzaro 'Magna Graecia' Catanzaro Italy.
                [2 ] Division of Innovative Clinical Trials, Department of Cardiology University Medical Center Göttingen (UMG) Göttingen Germany.
                [3 ] Applied Cachexia Research, Department of Cardiology Charité Medical School Berlin Germany.
                [4 ] Centre for Clinical and Basic Research IRCCS San Raffaele Pisana Rome Italy.
                [5 ] Institute of Research for Food Safety and Health (IRC-FSH)University of Catanzaro 'Magna Graecia'CatanzaroItaly; Centre for Clinical and Basic ResearchIRCCS San Raffaele PisanaRomeItaly.
                [6 ] Center for Stroke Research Charité Medical School, Campus Virchow- Klinikum Berlin Germany.
                Article
                Publisher Item ID: JCSM12116
                DOI: 10.1002/jcsm.12116
                PMC ID: 4864048
                PubMed ID: 27239419
                SO-VID: 3973ed0b-b531-42cd-83f5-d6ae9b15c12f
                History

                Keywords: Autophagy,Body composition,Cancer cachexia,Cardiac wasting,Heart failure,Megestrol acetate
                Data availability:
                Keywords: Autophagy, Body composition, Cancer cachexia, Cardiac wasting, Heart failure, Megestrol acetate

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