scholarly journals Impact of Cancer Cachexia on Cardiac and Skeletal Muscle: Role of Exercise Training

Cancers ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 342
Author(s):  
Cláudia Bordignon ◽  
Bethânia S. dos Santos ◽  
Daniela D. Rosa
Keyword(s):  
Cardiac Remodeling ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Clinical Evidence ◽  
Premature Death ◽  
Muscle Loss ◽  
Multimodal Approach ◽  
Progressive Loss

Cachexia is a multifactorial syndrome that presents with, among other characteristics, progressive loss of muscle mass and anti-cardiac remodeling effect that may lead to heart failure. This condition affects about 80% of patients with advanced cancer and contributes to worsening patients’ tolerance to anticancer treatments and to their premature death. Its pathogenesis involves an imbalance in metabolic homeostasis, with increased catabolism and inflammatory cytokines levels, leading to proteolysis and lipolysis, with insufficient food intake. A multimodal approach is indicated for patients with cachexia, with the aim of reducing the speed of muscle wasting and improving their quality of life, which may include nutritional, physical, pharmacologic, and psychological support. This review aims to outline the mechanisms of muscle loss, as well as to evaluate the current clinical evidence of the use of physical exercise in patients with cachexia.

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 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 Inhibition of the Fission Machinery Mitigates OPA1 Impairment in Adult Skeletal Muscles

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 597 ◽  
Author(s):  
Vanina Romanello ◽  
Marco Scalabrin ◽  
Mattia Albiero ◽  
Bert Blaauw ◽  
Luca Scorrano ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Skeletal Muscles ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Premature Death ◽  
Muscle Loss ◽  
Mitochondrial Network ◽  
Double Knockout ◽  
Physiological Relevance ◽  
Simultaneous Inhibition

The maintenance of muscle mass and its ability to function relies on a bioenergetic efficient mitochondrial network. This network is highly impacted by fusion and fission events. We have recently shown that the acute deletion of the fusion protein Opa1 induces muscle atrophy, systemic inflammatory response, precocious epithelial senescence, and premature death that are caused by muscle-dependent secretion of FGF21. However, both fusion and fission machinery are suppressed in aging sarcopenia, cancer cachexia, and chemotherapy-induced muscle wasting. We generated inducible muscle-specific Opa1 and Drp1 double-knockout mice to address the physiological relevance of the concomitant impairment of fusion and fission machinery in skeletal muscle. Here we show that acute ablation of Opa1 and Drp1 in adult muscle causes the accumulation of abnormal and dysfunctional mitochondria, as well as the inhibition of autophagy and mitophagy pathways. This ultimately results in ER stress, muscle loss, and the reduction of force generation. However, the simultaneous inhibition of the fission protein Drp1 when Opa1 is absent alleviates FGF21 induction, oxidative stress, denervation, and inflammation rescuing the lethal phenotype of Opa1 knockout mice, despite the presence of any muscle weakness. Thus, the simultaneous inhibition of fusion and fission processes mitigates the detrimental effects of unbalanced mitochondrial fusion and prevents the secretion of pro-senescence factors.

scholarly journals Muscle alterations in the development and progression of cancer-induced muscle atrophy: a review

2020 ◽  
Vol 128 (1) ◽  
pp. 25-41 ◽  
Author(s):  
Megan E. Rosa-Caldwell ◽  
Dennis K. Fix ◽  
Tyrone A. Washington ◽  
Nicholas P. Greene
Keyword(s):  
Cancer Patients ◽  
Protein Turnover ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Cell Function ◽  
Developmental Stages ◽  
Muscle Loss ◽  
Inflammatory Signaling ◽  
Mortality And Morbidity ◽  
Cancer Types

Cancer cachexia—cancer-associated body weight and muscle loss—is a significant predictor of mortality and morbidity in cancer patients across a variety of cancer types. However, despite the negative prognosis associated with cachexia onset, there are no clinical therapies approved to treat or prevent cachexia. This lack of treatment may be partially due to the relative dearth of literature on mechanisms occurring within the muscle before the onset of muscle wasting. Therefore, the purpose of this review is to compile the current scientific literature on mechanisms contributing to the development and progression of cancer cachexia, including protein turnover, inflammatory signaling, and mitochondrial dysfunction. We define “development” as changes in cell function occurring before the onset of cachexia and “progression” as alterations to cell function that coincide with the exacerbation of muscle wasting. Overall, the current literature suggests that multiple aspects of cellular function, such as protein turnover, inflammatory signaling, and mitochondrial quality, are altered before the onset of muscle loss during cancer cachexia and clearly highlights the need to study more thoroughly the developmental stages of cachexia. The studying of these early aberrations will allow for the development of effective therapeutics to prevent the onset of cachexia and improve health outcomes in cancer patients.

scholarly journals The Expanding Role of Real-World Evidence Trials in Health Care Decision Making

2019 ◽  
Vol 14 (1) ◽  
pp. 174-179 ◽  
Author(s):  
David C. Klonoff
Keyword(s):  
Real World ◽  
Clinical Evidence ◽  
Real World Data ◽  
Medical Products ◽  
Advantages And Disadvantages ◽  
Randomized Controlled ◽  
Real World Evidence ◽  
Care Decision

Real-world evidence (RWE) is the clinical evidence about benefits or risks of medical products derived from analyzing real world data (RWD), which are data collected through routine clinical practice. This article discusses the advantages and disadvantages of RWE studies, how these studies differ from randomized controlled trials (RCTs), how to overcome barriers to current skepticism about RWE, how FDA is using RWE, how to improve the quality of RWE, and finally the future of RWE trials.

scholarly journals Tumor Angiogenesis as a Target for Dietary Cancer Prevention

2012 ◽  
Vol 2012 ◽  
pp. 1-23 ◽  
Author(s):  
William W. Li ◽  
Vincent W. Li ◽  
Michelle Hutnik ◽  
Albert S. Chiou
Keyword(s):  
Quality Of Life ◽  
Cancer Prevention ◽  
Healthcare Costs ◽  
Clinical Evidence ◽  
Advanced Malignancies ◽  
Antiangiogenic Drugs ◽  
Novel Strategy ◽  
Kidney Liver

Between 2000 and 2050, the number of new cancer patients diagnosed annually is expected to double, with an accompanying increase in treatment costs of more than $80 billion over just the next decade. Efficacious strategies for cancer prevention will therefore be vital for improving patients' quality of life and reducing healthcare costs. Judah Folkman first proposed antiangiogenesis as a strategy for preventing dormant microtumors from progressing to invasive cancer. Although antiangiogenic drugs are now available for many advanced malignancies (colorectal, lung, breast, kidney, liver, brain, thyroid, neuroendocrine, multiple myeloma, myelodysplastic syndrome), cost and toxicity considerations preclude their broad use for cancer prevention. Potent antiangiogenic molecules have now been identified in dietary sources, suggesting that a rationally designed antiangiogenic diet could provide a safe, widely available, and novel strategy for preventing cancer. This paper presents the scientific, epidemiologic, and clinical evidence supporting the role of an antiangiogenic diet for cancer prevention.

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 CONDITION OF THE MUSCULOSKELETAL SYSTEM IN PATIENTSWITH ACROMEGALY.

2010 ◽  
Vol 13 (1) ◽  
pp. 19-27
Author(s):  
A S Fedotova ◽  
N N Molitvoslovova ◽  
L I Alekseeva ◽  
L Ya Rozhinskaya ◽  
A. S. Fedotova ◽  
...  
Keyword(s):  
Clinical Manifestations ◽  
Cochrane Collaboration ◽  
Premature Death ◽  
Social Adaptation ◽  
Mineral Density ◽  
Locomotor Apparatus ◽  
Low Incidence ◽  
Additional Therapy

Despite the relatively low incidence of acromegaly (60-70 cases per I million inhabitants), this disease has a special place among the heterogeneous group of diseases that lead to the defeat of the locomotor apparatus. The slow growth of the clinical manifestations of acromegaly and as a consequence, late diagnosis, the cause of early disability and premature death of patients. In order to improve the quality of life and social adaptation of patients to date is an obvious need to identify groups of patients with acromegaly, requiring additional therapy for osteoporosis and osteoarthritis. We performed the search in bibliographic bases MEDLINE and Cochrane Collaboration from 2000 on 2009. Key words were the following: acromegaly, acromegaly and arthropathy, osteoporosis and acromegaly, the bone mineral density and acromegaly, fractures and acromegaly. In this article the data about role of risk factors for the defeat ofosteoarticular apparatus, the dynamics of the articular syndrome and the state of bone tissue in acromegaly.

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