Palus, Sandra

[["dc.bibliographiccitation.firstpage","19"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","238"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Springer, J. I."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Anker, Stefan-D."],["dc.date.accessioned","2018-11-07T10:22:26Z"],["dc.date.available","2018-11-07T10:22:26Z"],["dc.date.issued","2017"],["dc.description.abstract","Approximately 40-50% of the population over 80 years of age suffers from sarcopenia making this condition a major geriatric clinical disorder and a key challenge to healthy aging. The hallmark symptom of sarcopenia is the loss of muscle mass and strength without the loss of overall body weight. Sarcopenic patients are likely to have worse clinical outcomes and higher mortality compared to healthy individuals. This review will focus on animal models designed to study sarcopenia including hind-limb unloading, de-nervation, and immobilization by using casts or wire strategies, as well as using aged rodents. Currently there are no registered treatments for sarcopenia. Most sarcopenic individuals show signs of physical frailty, which leads to increases the prevalence of balance disorders, falls, fractures and pain. Therefore, is it essential to develop and use relevant animal models to further the research on sarcopenia therapy? (C) 2017 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2017.03.152"],["dc.identifier.isi","000402478900004"],["dc.identifier.pmid","28465116"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42272"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Models of sarcopenia: Short review"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","jcsm.13009"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Elkina, Yulia"],["dc.contributor.author","Braun, Tanja"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Döhner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2022-06-01T09:39:03Z"],["dc.date.available","2022-06-01T09:39:03Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/jcsm.13009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108378"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.title","The erythropoietin‐derived peptide ARA 284 reduces tissue wasting and improves survival in a rat model of cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","97"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Musolino, Vincenzo"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Latouche, Celine"],["dc.contributor.author","Gliozzi, Micaela"],["dc.contributor.author","Bosco, Francesca"],["dc.contributor.author","Scarano, Federica"],["dc.contributor.author","Nucera, Saverio"],["dc.contributor.author","Carresi, Cristina"],["dc.contributor.author","Scicchitano, Miriam"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Jaisser, Frederic"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Mollace, Vincenzo"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.v6.1"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69800"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cardiac expression of neutrophil gelatinase-associated lipocalin in a model of cancer cachexia-induced cardiomyopathy"],["dc.title.alternative","Cardiac expression of NGAL in cancer cachexia-induced cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","594"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","605"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Pötsch, Mareike S."],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2021-06-01T10:50:56Z"],["dc.date.available","2021-06-01T10:50:56Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jcsm.12537"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17186"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86832"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","MT‐102 prevents tissue wasting and improves survival in a rat model of severe cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of cachexia, sarcopenia and muscle"],["dc.bibliographiccitation.lastpage","52"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Cvan Trobec, Katja"],["dc.contributor.author","Kerec Kos, Mojca"],["dc.contributor.author","Trontelj, Jurij"],["dc.contributor.author","Grabnar, Iztok"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Lainscak, Mitja"],["dc.date.accessioned","2019-07-09T11:42:33Z"],["dc.date.available","2019-07-09T11:42:33Z"],["dc.date.issued","2015-03-01"],["dc.description.abstract","BACKGROUND: Body wasting and cachexia change body composition and organ function, with effects on drug pharmacokinetics. The aim of this study was to investigate how cancer and cancer cachexia modify liver metabolism and renal drug elimination in rats. METHODS: Nine male Wistar-Han rats received a single oral dose of midazolam and propranolol (markers of hepatic metabolism), and 10 rats received single intravenous dose of iohexol, a marker of glomerular filtration rate. After drug delivery, multiple dried blood samples were obtained within 2 h post-dose to evaluate drug pharmacokinetic profiles. After baseline sampling (D0), rats were injected with tumour cells. Drug application and blood sampling were repeated when rats developed tumours (Day 5-D5), and when rats were severely cachectic (Day 10-D10). Clearance (CL) and volume of distribution (Vd) of drugs were assessed with non-linear mixed effects modelling. Weight and body composition were measured on D0 and D10 and were related to pharmacokinetic parameters. RESULTS: All three drugs showed non-significant trend towards increased CL and Vd on D5. On D10, midazolam and propranolol CL and midazolam Vd significantly decreased from baseline (-80.5%, -79.8%, and -72.0%, respectively, P < 0.05 for all). Iohexol CL decreased by 29.8% from baseline value on D10, which was related to body weight loss (Pearson's r = 0.837, P = 0.019). CONCLUSIONS: Hepatic metabolism and renal drug elimination are significantly reduced in cachexia, which could increase risk of dose-related adverse events."],["dc.identifier.doi","10.1002/jcsm.12012"],["dc.identifier.pmid","26136411"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13568"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58694"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Influence of cancer cachexia on drug liver metabolism and renal elimination in rats."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","377"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","378"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Drescher, C."],["dc.contributor.author","Pelgrim, Loes"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Baumgarten, A."],["dc.contributor.author","von Haehling, S."],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, J. I."],["dc.date.accessioned","2018-11-07T09:57:28Z"],["dc.date.available","2018-11-07T09:57:28Z"],["dc.date.issued","2015"],["dc.identifier.isi","000366200403455"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37162"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Febuxostat reduces cancer cachexia-induced cardiomyopathy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","154"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","159"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Hetzer, Roland"],["dc.contributor.author","Meyer, Rudolf"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2019-07-09T11:41:13Z"],["dc.date.available","2019-07-09T11:41:13Z"],["dc.date.issued","2015"],["dc.description.abstract","ackground Recently, it was shown that a knock-out (KO) of the polycomb histone methyltransferase Ezh2 leads to cardiac hypertrophy in mice, which was driven by the homeodom ain transcription factor Six1. Here, we analyzed the expression of Six1 and its regulating factor Ezh2 in cardiac tissue of pa- tients with end-stage dilative cardiomyopathy (DCM). Methods Tissue samples of patients with end-stage DCM (n = 35) were com- pared with control s (n = 12) for the protein expression of Ezh1, Ezh2, Six1, and a marker of protein expression p70S6K. Results Contrary to the Ezh2-KO mouse model, we found a down-regulation of Six1 (26%) and an up-regulation of Ezh2 (76%) in DCM hearts, (both P < 0.05). Expression of Ezh2 and Six1 did not correlate in human tissue (DCM: r 2 : 0.03, P = 0.31 and donor: r 2 : 0.05, P = 0.45). Expression of Six1 weakly correlated with left ventricula r end-systolic diameter and fractional shortening. In DCM, Six1 also showed a positive correlation to the expression of the ribosomal protein p70S6K (r: 0.39, P = 0.02 9), which is involved in pro- tein synthesis. This correlation was not seen in donor tissue, whic h showed a trend for a negative correlation (r: 0.49, P = 0.08 ). Conclusion Our data indicate that the Ezh2/Six1 axis might be involved in human DCM. However, Six1 expression may be regulated by factors other t han Ezh2, and more research is needed to determine the precise role of Ezh2/Six1 in human DCM."],["dc.identifier.doi","10.1002/ehf2.12017"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11849"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58375"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Six1 is down-regulated in end-stage human dilated cardiomyopathy independently of Ezh2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","312"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","317"],["dc.bibliographiccitation.volume","218"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Hatanaka, Michiyoshi"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T10:09:59Z"],["dc.date.available","2018-11-07T10:09:59Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Erythropoietin administration, which is clinically used in cancer patients with cancer-induced anemia, has also potentially beneficial effects on nonhematopoietic organs. We assessed the effects of erythropoietin on cancer cachexia progression and cardiac wasting compared with placebo using the Yoshida hepatoma model. Methods: Wistar rats were divided in a sham group (n = 10) and a tumor-bearing group (n = 60). The tumor-bearing group was further randomized to placebo (n = 28), 500 Unit/kg/day (n = 16) or 5000 Unit/kg/day of erythropoietin (n = 16). Body composition was measured using nuclear magnetic resonance spectroscopy, cardiac function using echocardiography, physical activity using infrared monitoring system. Results: Tumor-bearing rats with high dose erythropoietin led to a significant improvement on survival compared with placebo (hazard ratio: 0.43, 95% CI: 0.20-0.92, p = 0.030), though low dose erythropoietin did not reach significance (hazard ratio: 0.46, 95% CI: 0.22-1.02, p = 0.056). Loss of body weight, wasting of lean mass, fat mass, and reduced physical activity were ameliorated in rats treated with both low and high doses of erythropoietin (p < 0.05, all). Moreover, reduced left ventricularmass and left ventricular systolic function were also ameliorated in rats treated with low and high doses of erythropoietin (p < 0.05, respectively). Conclusions: Overall, the present data support that cardiac wasting induced by cancer cachexia plays an important rolewhich leads to impaired survival, provided that the erythropoietin could be an effective therapeutic approach for cancer cachexia progression and cardiac wasting. (C) 2016 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ijcard.2016.05.008"],["dc.identifier.isi","000377856300052"],["dc.identifier.pmid","27240157"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39764"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1874-1754"],["dc.relation.issn","0167-5273"],["dc.title","Erythropoietin improves cardiac wasting and outcomes in a rat model of liver cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","174"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","180"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Pelgrim, Loes"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Baumgarten, Anna"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T09:56:41Z"],["dc.date.available","2018-11-07T09:56:41Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Activity of xanthine oxidase is induced in cancer cachexia, and its inhibition by allopurinol or oxypurinol improves survival and reduces wasting in the Yoshida hepatoma cancer cachexia model. Here, we tested the effects of the second-generation xanthine oxidase inhibitor febuxostat compared with placebo in the same model as used previously by our group. Methods Wistar rats (similar to 200g) were treated daily with febuxostat at 5mg/kg/day or placebo via gavage for a maximum of 17days. Weight change, quality of life, and body composition were analysed. After sacrifice, proteasome activity in the gastrocnemius muscle was measured. Muscle-specific proteins involved in metabolism were analysed by western blotting. Results Treatment of the tumour-bearing rats with febuxostat led to a significantly improved survival compared with placebo (hazard ratio: 0.45, 95% confidence interval: 0.22-0.93, P=0.03). Loss of body weight was reduced (-26.312.4g) compared with placebo (-50.2 +/- 2.1g, P<0.01). Wasting of lean mass was attenuated (-12.7 +/- 10.8g) vs. placebo (-31.9 +/- 2.1g, P<0.05). While we did not see an effect of febuxostat on proteasome activity at the end of the study, the pAkt/Akt ratio was improved by febuxostat (0.94 +/- 0.09) vs. placebo (0.41 +/- 0.05, P<0.01), suggesting an increase in protein synthesis. Conclusions Febuxostat attenuated cachexia progression and improved survival of tumour-bearing rats."],["dc.description.sponsorship","Sumitomo Life Welfare and Culture Foundation"],["dc.identifier.doi","10.1002/jcsm.12017"],["dc.identifier.isi","000355340500007"],["dc.identifier.pmid","26136193"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37010"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Febuxostat improves outcome in a rat model of cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","555"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","566"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Musolino, Vincenzo"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Drescher, Cathleen"],["dc.contributor.author","Gliozzi, Micaela"],["dc.contributor.author","Carresi, Cristina"],["dc.contributor.author","Vitale, Cristiana"],["dc.contributor.author","Muscoli, Carolina"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Mollace, Vincenzo"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2019-07-09T11:42:54Z"],["dc.date.available","2019-07-09T11:42:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Background 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. Anticachectic 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. Methods In this study the effects of MA were tested in cachectic tumour-bearing rats (Yoshida AH-130 ascites hepatoma). Rats were treated daily with 100 mg/kg of MA or placebo starting one day after tumour inoculation, and for a period of 16 days. Body weight and body composition were assessed at baseline and at the end of the study. Cardiac function was analysed by echocardiography at baseline and at day 11. Locomotor activity and food intake were assessed before tumour inoculation and at day 11. Autophagic markers were assessed in gastrocnemius muscle and heart by western blot analysis. Results Treatment with 100 mg/kg/day MA significantly attenuated the loss of body weight ( 9 ± 12%, P<0.05) and the wasting of lean and fat mass ( 7.0 ± 6% and 22.4 ± 3 %, P<0.001 and P<0.05, respectively). Administration of 100 mg/kg/day MA significantly protected the heart from general atrophy (633.8 ± 30mg vs. placebo 474 ± 13 mg, P<0.001). Tumour-bearing rats displayed cardiac dysfunction, as indicated by the significant impairment of the left ventricular ejection fraction, the left ventricular fractional shortening, the stroke volume, the end dyastolic volume, and the end systolic volume. In contrast, MA significantly improved left ventricular ejection fraction, left ventricular fractional shortening, and left ventricular end systolic volume. Western blotting analysis showed an upregulation of the autophagic pathway in the gastrocnemius and hearts of the placebo-treated tumour-bearing rats. Treatment with MA, however, was able to modulate the autophagic markers (e.g. Beclin-1, p62, TRAF6, and LC3) in the gastrocnemius and in the hearts of tumourbearing rats. Most importantly, 100 mg/kg/day MA reduced mortality [hazard ratio (HR): 0.44; 95%CI: 0.20–1.00; P = 0.0486]. Conclusions Megestrol acetate improved survival and reduced wasting through a marked downregulation of autophagy, occurring in both skeletal and heart muscle, the latter effect leading to a significant improvement of cardiac function. Our data suggest thatMA might represent a valuable strategy to counteract the development of cancer cachexia-induced cardiomyopathy."],["dc.identifier.doi","10.1002/jcsm.12116"],["dc.identifier.pmid","27239419"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58781"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Megestrol acetate improves cardiac function in a model of cancer cachexia-induced cardiomyopathy by autophagic modulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]