Cancer cachexia is characterized by a continuous loss of locomotor skeletal muscle mass, which causes profound muscle weakness. If this atrophy and weakness also occurs in diaphragm muscle, it could lead to respiratory failure, which is a major cause of death in patients with cancer. Thus, the purpose of the current study was to determine whether colon-26 (C-26) cancer cachexia causes diaphragm muscle fiber atrophy and weakness and compromises ventilation. All diaphragm muscle fiber types were significantly atrophied in C-26 mice compared to controls, and the atrophy-related genes, atrogin-1 and MuRF1, significantly increased. Maximum isometric specific force of diaphragm strips, absolute maximal calcium activated force, and maximal specific calcium-activated force of permeabilized diaphragm fibers were all significantly decreased in C-26 mice compared to controls. Further, isotonic contractile properties of the diaphragm were affected to an even greater extent than isometric function. Ventilation measurements demonstrated that C-26 mice have a significantly lower tidal volume compared to controls under basal conditions and, unlike control mice, an inability to increase breathing frequency, tidal volume, and, thus, minute venti...Continue Reading
Associated Clinical Trials
Shortening velocity extrapolated to zero load and unloaded shortening velocity of whole rat skeletal muscle
The effect of calcium on the maximum velocity of shortening in skinned skeletal muscle fibres of the rabbit
Force-velocity properties of human skeletal muscle fibres: myosin heavy chain isoform and temperature dependence
Rate constant of muscle force redevelopment reflects cooperative activation as well as cross-bridge kinetics
Use of the rapid/shallow breathing index as an indicator of patient work of breathing during pressure support ventilation
Dystrophin glycoprotein complex dysfunction: a regulatory link between muscular dystrophy and cancer cachexia
Activity of the Akt-dependent anabolic and catabolic pathways in muscle and liver samples in cancer-related cachexia
Daily physical-rest activities in relation to nutritional state, metabolism, and quality of life in cancer patients with progressive cachexia
Increased expression of phosphorylated forms of RNA-dependent protein kinase and eukaryotic initiation factor 2alpha may signal skeletal muscle atrophy in weight-losing cancer patients.
TNF-alpha acts via TNFR1 and muscle-derived oxidants to depress myofibrillar force in murine skeletal muscle
Hsp70 overexpression inhibits NF-kappaB and Foxo3a transcriptional activities and prevents skeletal muscle atrophy.
Effects of submaximal activation on the determinants of power of chemically skinned rat soleus fibres
Calculation of muscle maximal shortening velocity by extrapolation of the force-velocity relationship: afterloaded versus isotonic release contractions
STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia
Pharmacological strategies in lung cancer-induced cachexia: effects on muscle proteolysis, autophagy, structure, and weakness
MicroRNA expression and protein acetylation pattern in respiratory and limb muscles of Parp-1(-/-) and Parp-2(-/-) mice with lung cancer cachexia
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Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia
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Treating cachexia using soluble ACVR2B improves survival, alters mTOR localization, and attenuates liver and spleen responses
The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin-6
Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching
Colon 26 adenocarcinoma (C26)-induced cancer cachexia impairs skeletal muscle mitochondrial function and content
Skeletal myofiber VEGF deficiency leads to mitochondrial, structural, and contractile alterations in mouse diaphragm.
IL-8 Released from Human Pancreatic Cancer and Tumor-Associated Stromal Cells Signals through a CXCR2-ERK1/2 Axis to Induce Muscle Atrophy
Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle.
Physiological and functional failure in chronic obstructive pulmonary disease, congestive heart failure and cancer: a debilitating intersection of sarcopenia, cachexia and breathlessness
Pathophysiological mechanisms explaining poor clinical outcome of older cancer patients with low skeletal muscle mass.
Mitochondrial respiration and H2 O2 emission in saponin-permeabilized murine diaphragm fibers: optimization of fiber separation and comparison to limb muscle
Janus kinase inhibition prevents cancer- and myocardial infarction-mediated diaphragm muscle weakness in mice
Trabectedin and Lurbinectedin Extend Survival of Mice Bearing C26 Colon Adenocarcinoma, without Affecting Tumor Growth or Cachexia
Dissecting the role of the myofilament in diaphragm dysfunction during the development of heart failure in mice
Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness
Hyperbaric Oxygen Treatment Following Mid-Cervical Spinal Cord Injury Preserves Diaphragm Muscle Function.
NAD(P)H oxidase subunit p47phox is elevated, and p47phox knockout prevents diaphragm contractile dysfunction in heart failure
Is Mitochondrial Oxidative Stress the Key Contributor to Diaphragm Atrophy and Dysfunction in Critically Ill Patients?
Increased tumour burden alters skeletal muscle properties in the KPC mouse model of pancreatic cancer.
MEF2c-dependent downregulation of Myocilin mediates cancer-induced muscle wasting and associates with cachexia in cancer patients
Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia.
Targeting the Activin Receptor Signaling to Counteract the Multi-Systemic Complications of Cancer and Its Treatments.
Cachexia & Brown Fat
Cachexia is a condition associated with progressive weight loss due to severe illness. In cancer patients, it is proposed to occur as a result of tumor-induced energy wasting. Several proteins have been implicated in browning and depletion of white adipose tissue. Here is the latest research on cachexia and brown fat.
Cardiac cachexia is a syndrome associated with the progressive loss of muscle and fat mass. It most commonly affects patients with heart failure and can significantly decrease the quality of life and survival in these patients. Here is the latest research on cardiac cachexia.