Preventive effects of low‐intensity exercise on cancer cachexia–induced muscle atrophy

Tanaka, Minoru; Sugimoto, Ken; Fujimoto, Taku; Xie, Kaizhou; Takahashi, Toshimasa; Akasaka, Hiroshi; Kurinami, Hitomi; Yasunobe, Yukiko; Matsumoto, Tomohiro; Fujino, Hidemi; Rakugi, Hiromi

doi:10.1096/fj.201802430r

Cited by 29 publications

(43 citation statements)

References 48 publications

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“…Furthermore, some previous studies revealed that autophagic proteolysis is involved in cancer cachexia-induced muscle atrophy [9][10][11]. In contrast, the expression of molecules related to protein synthesis, including insulin-like growth factor 1 (IGF-1) and phosphorylated mechanistic target of rapamycin (mTOR), is suppressed in cachectic muscles [12]. It was also demonstrated that redox homeostasis balances protein synthesis and degradation in skeletal muscles during cancer cachexia [13,14].…”

Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Ameliorates Cancer Cachexia-Induced Muscle Wasting through Adiponectin Signaling

Morinaga

Sako

Isobe

et al. 2021

IJMS

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Cachexia is a multifactorial syndrome characterized by muscle loss that cannot be reversed by conventional nutritional support. To uncover the molecular basis underlying the onset of cancer cachectic muscle wasting and establish an effective intervention against muscle loss, we used a cancer cachectic mouse model and examined the effects of aerobic exercise. Aerobic exercise successfully suppressed muscle atrophy and activated adiponectin signaling. Next, a cellular model for cancer cachectic muscle atrophy using C2C12 myotubes was prepared by treating myotubes with a conditioned medium from a culture of colon-26 cancer cells. Treatment of the atrophic myotubes with recombinant adiponectin was protective against the thinning of cells through the increased production of p-mTOR and suppression of LC3-II. Altogether, these findings suggest that the activation of adiponectin signaling could be part of the molecular mechanisms by which aerobic exercise ameliorates cancer cachexia-induced muscle wasting.

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Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Ameliorates Cancer Cachexia-Induced Muscle Wasting through Adiponectin Signaling

Morinaga

Sako

Isobe

et al. 2021

IJMS

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“…There are several protective and therapeutic measures against muscular atrophy, such as intake of essential amino acids (8), insulin-like growth factor (IGF)-I treatment (9) and anabolic androgenic steroids (10); however, these measures can cause increased drug resistance and cardiac events, limiting their therapeutic utility for the treatment of muscle atrophy (4,11). Although major advances in our understanding of protein loss in muscle atrophy have been made recently (12–15), it is important to elucidate the underlying molecular regulatory mechanisms of dysfunctional muscle anabolism during skeletal muscle atrophy, in order to develop promising strategies to prevent and treat muscular atrophy.…”

Section: Introductionmentioning

confidence: 99%

Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo

et al. 2019

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Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin-1 were increased, both in vitro and in vivo. The impact of starvation on the expression patterns of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) was next determined. The expression patterns of miR-23a, miR-206 and miR-27b in the starved mice exhibited similar trends as those in starved C2C12 cells in vitro, whereas the expression patterns of six other miRNAs (miR-18a, miR-133a, miR-133b, miR-186, miR-1a and miR-29b) differed between the in vivo and the in vitro starvation models. The present study indicated that in vitro expression of the selected miRNAs was not completely consistent with that in vivo. By contrast, lncRNAs showed excellent consistency in their expression patterns in both the in vitro and in vivo starvation models; six of the lncRNAs (Atrolnc-1, long intergenic non-protein coding RNA of muscle differentiation 1, Myolinc, lncRNA myogenic differentiation 1, Dum and muscle anabolic regulator 1) were significantly elevated in starved tissues and cells, while lnc-mg was significantly decreased, compared with the control groups. Thus, lncRNAs involved in muscle atrophy have the potential to be developed as diagnostic tools.

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“…in contrast, resistance training induced the expression of genes related to muscle damage and repair, such as myogenin and iGF-ieb, which might be due to the excessive stress caused by the high resistance load in the tumor-bearing state (147). in addition, Tanaka et al (148) discovered that low-intensity exercise inhibited Yoshida aH130 ascites lc cell-induced cancer cachexia through the skeletal uPS in male Wistar rats. in addition, low-intensity exercise increased the levels of hypoxia-inducible factor-1α and p-aMPK, which suppressed the loss of muscle mass and the inactivation of mTor in the soleus muscle.…”

Section: Treatment Of Muscle Atrophy Caused By Cancer Cachexiamentioning

confidence: 99%

Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review)

Huang

et al. 2020

Mol Med Rep

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Muscle atrophy is a severe clinical problem involving the loss of muscle mass and strength that frequently accompanies the development of numerous types of cancer, including pancreatic, lung and gastric cancers. cancer cachexia is a multifactorial syndrome characterized by a continuous decline in skeletal muscle mass that cannot be reversed by conventional nutritional therapy. The pathophysiological characteristic of cancer cachexia is a negative protein and energy balance caused by a combination of factors, including reduced food intake and metabolic abnormalities. numerous necessary cellular processes are disrupted by the presence of abnormal metabolites, which mediate several intracellular signaling pathways and result in the net loss of cytoplasm and organelles in atrophic skeletal muscle during various states of cancer cachexia. currently, the clinical morbidity and mortality rates of patients with cancer cachexia are high. once a patient enters the cachexia phase, the consequences are difficult to reverse and the treatment methods for cancer cachexia are very limited. The present review aimed to summarize the recent discoveries regarding the pathogenesis of cancer cachexia-induced muscle atrophy and provided novel ideas for the comprehensive treatment to improve the prognosis of affected patients. Contents 1. introduction 2. activation of the uPS 3. Induction of proinflammatory factors 4. regulation of signaling pathways, transcription factors and micrornas (mirnas/mirs) 5. cell autophagy/lysosomal and ca 2+-dependent protein degradation pathways 6. endoplasmic reticulum stress and mitochondrial dysfunction 7. other receptors and substances that affect metabolism 8. Treatment of muscle atrophy caused by cancer cachexia 9. conclusion

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Preventive effects of low‐intensity exercise on cancer cachexia–induced muscle atrophy

Cited by 29 publications

References 48 publications

Aerobic Exercise Ameliorates Cancer Cachexia-Induced Muscle Wasting through Adiponectin Signaling

Aerobic Exercise Ameliorates Cancer Cachexia-Induced Muscle Wasting through Adiponectin Signaling

Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo

Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review)

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