Erythropoietin attenuates cachectic events and decreases production of interleukin-6, a cachexia-inducing cytokine

Kanzaki, Masaki; Soda, Kuniyasu; Gin, Pham Tien; Kai, Toshihiro; Konishi, Fumio; Kawakami, Masanobu

doi:10.1016/j.cyto.2005.10.002

Cited by 32 publications

(21 citation statements)

References 20 publications

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“…Anemia is an important component of the wasting process, since erythropoietin administered to tumor-bearing mice can decrease circulating IL-6 levels, improve anemia, and delay the wasting process (21). Since maximal running velocity appeared to be an important predictor of future muscle mass loss, we looked to see whether there was a relationship with the development of anemia.…”

Section: Discussionmentioning

confidence: 99%

Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice

Baltgalvis

Berger

Peña

et al. 2010

Journal of Applied Physiology

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Criteria for diagnosing cachexia in adults include unintentional loss in body weight, decreased strength, fatigue, anorexia, and low muscle mass. Cachexia is also associated with systemic inflammation, altered metabolism, and anemia. The Apc(Min/+) mouse is a model of cachexia directly related to intestinal tumor burden and subsequent chronic inflammation. These mice also demonstrate muscle weakness, fatigue, decreased volitional activity, and elevated circulating IL-6 levels. The purpose of this study was to determine the time course of changes in physical activity and their relationship to anemia, muscle apoptosis, and muscle mass and body mass loss during cachexia. A subset of male Apc(Min/+) mice were given access to voluntary activity wheels from 5 to 26 wk of age, while sedentary male Apc(Min/+) mice were housed in cages lacking wheels. At the study's end mice were stratified by cachectic symptoms. Severely cachectic mice had decreased wheel running performance at 15 wk of age, while anemia and body weight loss were not present until 18 wk of age. Severely cachectic mice had lower hemoglobin levels compared with mildly cachectic mice at 13, 18, and 22 wk of age. Severely cachectic mice also demonstrated threefold more BCL2-associated X protein (BAX) protein in the gastrocnemius muscle at 26 wk of age compared with mildly cachectic mice. In sedentary Apc(Min/+) mice at 26 wk of age anemia was present, and markers of apoptosis were induced in severely cachectic muscle. Proapoptotic protein expression was induced in both red and white portions of gastrocnemius muscle as well as in soleus muscle of severely cachectic mice compared with mildly cachectic mice. These data demonstrate that decrements in wheel running performance precede loss of body mass and that inherent muscle oxidative capacity is not protective against muscle apoptosis.

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Section: Discussionmentioning

confidence: 99%

Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice

Baltgalvis

Berger

Peña

et al. 2010

Journal of Applied Physiology

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“…It is possible that physical activity levels are reduced because of the onset of anemia. In fact, others have shown that erythropoietin administration improves symptoms of cachexia, and decreases circulating IL-6 levels (25). …”

Section: Exercise Il-6 and Cachexiamentioning

confidence: 99%

Interleukin 6 as a Key Regulator of Muscle Mass during Cachexia

Carson

Baltgalvis

2010

Exercise and Sport Sciences Reviews

190

197

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“…Other drugs that are investigated to be used for cancer cachexia include Erythropoetin [171][172][173] , ACE inhibitors [174] , and β-blockers [175] .…”

Section: Othersmentioning

confidence: 99%

Cancer cachexia, mechanism and treatment

Aoyagi¹,

Terracina²,

Ali³

et al. 2015

WJGO

376

282

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It is estimated that half of all patients with cancer eventually develop a syndrome of cachexia, with anorexia and a progressive loss of adipose tissue and skeletal muscle mass. Cancer cachexia is characterized by systemic inflammation, negative protein and energy balance, and an involuntary loss of lean body mass. It is an insidious syndrome that not only has a dramatic impact on patient quality of life, but also is associated with poor responses to chemotherapy and decreased survival. Cachexia is still largely an underestimated and untreated condition, despite the fact that multiple mechanisms are reported to be involved in its development, with a number of cytokines postulated to play a role in the etiology of the persistent catabolic state. Existing therapies for cachexia, including orexigenic appetite stimulants, focus on palliation of symptoms and reduction of the distress of patients and families rather than prolongation of life. Recent therapies for the cachectic syndrome involve a multidisciplinary approach. Combination therapy with diet modification and/or exercise has been added to novel pharmaceutical agents, such as Megestrol acetate, medroxyprogesterone, ghrelin, omega-3-fatty acid among others. These agents are reported to have improved survival rates as well as quality of life. In this review, we will discuss the emerging understanding of the mechanisms of cancer cachexia, the current treatment options including multidisciplinary combination therapies, as well an update on new and ongoing clinical trials.

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Erythropoietin attenuates cachectic events and decreases production of interleukin-6, a cachexia-inducing cytokine

Cited by 32 publications

References 20 publications

Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice

Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice

Interleukin 6 as a Key Regulator of Muscle Mass during Cachexia

Cancer cachexia, mechanism and treatment

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Erythropoietin attenuates cachectic events and decreases production of interleukin-6, a cachexia-inducing cytokine

Cited by 32 publications

References 20 publications

Activity level, apoptosis, and development of cachexia in ApcMin/+ mice

Activity level, apoptosis, and development of cachexia in ApcMin/+ mice

Interleukin 6 as a Key Regulator of Muscle Mass during Cachexia

Cancer cachexia, mechanism and treatment

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Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice

Activity level, apoptosis, and development of cachexia in Apc^Min/+ mice