The role of cytokines in muscle wasting: Its relation with cancer cachexia

1992 ◽  
Vol 12 (6) ◽  
pp. 637-652 ◽  
Author(s):  
Josep M. Argilés ◽  
Cèlia Garcia-Martínez ◽  
Maria Llovera ◽  
Francisco J. López-Soriano
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting

scholarly journals Nutraceuticals and Exercise against Muscle Wasting during Cancer Cachexia

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2536
Author(s):  
Giorgio Aquila ◽  
Andrea David Re Cecconi ◽  
Jeffrey J. Brault ◽  
Oscar Corli ◽  
Rosanna Piccirillo
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscles ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Premature Death ◽  
Preclinical Studies ◽  
Current State ◽  
Causal Therapy ◽  
And Oxidative Stress

Cancer cachexia (CC) is a debilitating multifactorial syndrome, involving progressive deterioration and functional impairment of skeletal muscles. It affects about 80% of patients with advanced cancer and causes premature death. No causal therapy is available against CC. In the last few decades, our understanding of the mechanisms contributing to muscle wasting during cancer has markedly increased. Both inflammation and oxidative stress (OS) alter anabolic and catabolic signaling pathways mostly culminating with muscle depletion. Several preclinical studies have emphasized the beneficial roles of several classes of nutraceuticals and modes of physical exercise, but their efficacy in CC patients remains scant. The route of nutraceutical administration is critical to increase its bioavailability and achieve the desired anti-cachexia effects. Accumulating evidence suggests that a single therapy may not be enough, and a bimodal intervention (nutraceuticals plus exercise) may be a more effective treatment for CC. This review focuses on the current state of the field on the role of inflammation and OS in the pathogenesis of muscle atrophy during CC, and how nutraceuticals and physical activity may act synergistically to limit muscle wasting and dysfunction.

scholarly journals MicroRNAs in Skeletal Muscle and Hints on Their Potential Role in Muscle Wasting During Cancer Cachexia

2020 ◽  
Vol 10 ◽  
Author(s):  
Gioacchino P. Marceca ◽  
Giovanni Nigita ◽  
Federica Calore ◽  
Carlo M. Croce
Keyword(s):  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Phenotypic Alteration ◽  
Specific Tumor ◽  
Non Coding Rnas

Cancer-associated cachexia is a heterogeneous, multifactorial syndrome characterized by systemic inflammation, unintentional weight loss, and profound alteration in body composition. The main feature of cancer cachexia is represented by the loss of skeletal muscle tissue, which may or may not be accompanied by significant adipose tissue wasting. Such phenotypic alteration occurs as the result of concomitant increased myofibril breakdown and reduced muscle protein synthesis, actively contributing to fatigue, worsening of quality of life, and refractoriness to chemotherapy. According to the classical view, this condition is primarily triggered by interactions between specific tumor-induced pro-inflammatory cytokines and their cognate receptors expressed on the myocyte membrane. This causes a shift in gene expression of muscle cells, eventually leading to a pronounced catabolic condition and cell death. More recent studies, however, have shown the involvement of regulatory non-coding RNAs in the outbreak of cancer cachexia. In particular, the role exerted by microRNAs is being widely addressed, and several mechanistic studies are in progress. In this review, we discuss the most recent findings concerning the role of microRNAs in triggering or exacerbating muscle wasting in cancer cachexia, while mentioning about possible roles played by long non-coding RNAs and ADAR-mediated miRNA modifications.

scholarly journals Role of Exosomal MicroRNAs and myomiRs in the Development of Cancer Cachexia-Associated Muscle Wasting

2018 ◽  
Vol 4 ◽  
Author(s):  
Rodolfo Marinho ◽  
Paulo S. M. Alcântara ◽  
José P. Ottoch ◽  
Marilia Seelaender
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting

scholarly journals Neurohypophyseal hormones and skeletal muscle: a tale of two faces

2020 ◽  
Vol 30 (1) ◽  
pp. 53-57
Author(s):  
Alexandra Benoni ◽  
Alessandra Renzini ◽  
Giorgia Cavioli ◽  
Sergio Adamo
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Striated Muscle ◽  
Cardiac Atrophy ◽  
Neurohypophyseal Hormones

The neurohypophyseal hormones vasopressin and oxytocin were invested, in recent years, with novel functions upon striated muscle, regulating its differentiation, trophism, and homeostasis. Recent studies highlight that these hormones not only target skeletal muscle but represent novel myokines. We discuss the possibility of exploiting the muscle hypertrophying activity of oxytocin to revert muscle atrophy, including cancer cachexia muscle wasting. Furthermore, the role of oxytocin in cardiac homeostasis and the possible role of cardiac atrophy as a concause of death in cachectic patients is discussed.

scholarly journals MMP12 Knockout Prevent Weight and Muscle Loss Induced by Cancer Cachexia

2021 ◽  
Author(s):  
Lingbi Jiang ◽  
Mingming Yang ◽  
Shihui He ◽  
Zhengyang Li ◽  
Haobin Li ◽  
...  
Keyword(s):  
Weight Loss ◽  
Interleukin 6 ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Critical Role ◽  
Muscle Loss ◽  
Glycolipid Metabolism ◽  
Patients With Cancer

AbstractWeight loss and muscle wasting can have devastating impacts on survival and quality of life of patients with cancer cachexia. Here, we have established a hybrid mouse of ApcMin/+ mice and MMP12 knockout mice (ApcMin/+; MMP12-/-) and found that knockout MMP12 can suppress the weight and muscle loss of ApcMin/+ mice. In detail, we found that interleukin 6 was highly upregulated in the serum of cancer patients and MMP12 was increased in muscle of tumor-bearing mice. Interestingly, the interleukin 6 secreted by tumor cells led to MMP12 overexpression in the macrophages, which further resulted in degradation of insulin and insulin-like growth factor 1 and interruption of glycolipid metabolism. Notably, depletion of MMP12 prevented weight loss of ApcMin/+ mice. Our study uncovers the critical role of MMP12 in controlling weight and highlights the great potential of MMP12 in the treatment of cancer cachexia.

scholarly journals Role of myokines and osteokines in cancer cachexia

2021 ◽  
pp. 153537022110092
Author(s):  
Fabrizio Pin ◽  
Lynda F Bonewald ◽  
Andrea Bonetto
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Lipid Mediator ◽  
Promising Strategy ◽  
Different Types ◽  
Ultimate Cause ◽  
Endocrine Factors ◽  
Shed Light

Cancer-induced muscle wasting, i.e. cachexia, is associated with different types of cancer such as pancreatic, colorectal, lung, liver, gastric and esophageal. Cachexia affects prognosis and survival in cancer, and it is estimated that it will be the ultimate cause of death for up to 30% of cancer patients. Musculoskeletal alterations are known hallmarks of cancer cachexia, with skeletal muscle atrophy and weakness as the most studied. Recent evidence has shed light on the presence of bone loss in cachectic patients, even in the absence of bone-metastatic disease. In particular, we and others have shown that muscle and bone communicate by exchanging paracrine and endocrine factors, known as myokines and osteokines. This review will focus on describing the role of the most studied myokines, such as myostatin, irisin, the muscle metabolite β-aminoisobutyric acid, BAIBA, and IL-6, and osteokines, including TGF-β, osteocalcin, sclerostin, RANKL, PTHrP, FGF23, and the lipid mediator, PGE2 during cancer-induced cachexia. The interplay of muscle and bone factors, together with tumor-derived soluble factors, characterizes a complex clinical scenario in which musculoskeletal alterations are amongst the most debilitating features. Understanding and targeting the “secretome” of cachectic patients will likely represent a promising strategy to preserve bone and muscle during cancer cachexia thereby enhancing recovery.

scholarly journals Inhibition of HSP90 reversed STAT3 mediated muscle wasting induced by cancer cachexia

2021 ◽  
Author(s):  
Mengyuan Niu ◽  
Shiyu Song ◽  
Zhonglan Su ◽  
Lulu Wei ◽  
Li Li ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Therapeutic Potential ◽  
Mechanistic Study ◽  
Dependent Manner ◽  
Mice Model ◽  
Common Causes

AbstractCancer cachexia is one of the most common causes of death among cancer patients, no effective anti-cachectic treatment is currently available. In experimental cachectic models, aberrant activation of STAT3 in skeletal muscle has been found to contribute to muscle wasting. However, its clinical association, the factors regulating STAT3 activation, and the molecular mechanisms of STAT3-induced muscle atrophy in cancer cachexia remain incompletely understood. Here, we show that an enhanced interaction between STAT3 and HSP90, which causes the persistent STAT3 activation in the skeletal muscle of cancer cachexia patients, is the crucial event for the development of cachectic muscle wasting. Administration of HSP90 inhibitors alleviated the muscle wasting in C26 tumor-bearing cachetic mice model or C26 conditional medium induced C2C12 myotube atrophy. A mechanistic study indicated that in cachectic skeletal muscle, prolonged STAT3 activation triggered muscle wasting in a FOXO1-dependent manner, STAT3 activated FOXO1 by binding directly to its promoter. Our results provide key insights into the role of the HSP90/STAT3/FOXO1 axis in cachectic muscle wasting, which shows promising therapeutic potential as a target for the treatment of cancer cachexia.

Sign in / Sign up

Export Citation Format

Share Document