Cancer cachexia is a complex metabolic syndrome that is characterized by the loss of skeletal muscle mass and weakness, which compromises physical function, reduces quality of life, and ultimately can lead to mortality. Experimental models of cancer cachexia have recapitulated this skeletal muscle atrophy and consequent decline in muscle force generating capacity. However, more recently, we provided evidence that during severe cancer cachexia muscle weakness in the diaphragm muscle cannot be entirely accounted for by the muscle atrophy. This indicates that muscle weakness is not just a consequence of muscle atrophy but that there is also significant contractile dysfunction. The current study aimed to determine whether contractile dysfunction is also present in limb muscles during severe Colon-26 (C26) carcinoma cachexia by studying the glycolytic extensor digitorum longus (EDL) muscle and the oxidative soleus muscle, which has an activity pattern that more closely resembles the diaphragm. Severe C-26 cancer cachexia caused significant muscle fiber atrophy and a reduction in maximum absolute force in both the EDL and soleus muscles. However, normalization to muscle cross sectional area further demonstrated a 13% decrease in maxi...Continue Reading
Dystrophin glycoprotein complex dysfunction: a regulatory link between muscular dystrophy and cancer cachexia
Oxidative phenotype protects myofibers from pathological insults induced by chronic heart failure in mice
Morphology, metabolism, microcirculation, and strength of skeletal muscles in cancer-related cachexia
Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle.
Molecular, cellular and physiological characterization of the cancer cachexia-inducing C26 colon carcinoma in mouse.
Inhibition of FoxO transcriptional activity prevents muscle fiber atrophy during cachexia and induces hypertrophy.
Importance of functional and metabolic impairments in the characterization of the C-26 murine model of cancer cachexia.
Muscle wasting as main evidence of energy impairment in cancer cachexia: future therapeutic approaches
Tumor growth increases neuroinflammation, fatigue and depressive-like behavior prior to alterations in muscle function
Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia
Arginine depletion by arginine deiminase does not affect whole protein metabolism or muscle fractional protein synthesis rate in mice
Oxidative stress-induced dysregulation of excitation-contraction coupling contributes to muscle weakness
The regulation of skeletal muscle fatigability and mitochondrial function by chronically elevated interleukin-6
Colon 26 adenocarcinoma (C26)-induced cancer cachexia impairs skeletal muscle mitochondrial function and content
The myonuclear domain is not maintained in skeletal muscle during either atrophy or programmed cell death
Distinct cachexia profiles in response to human pancreatic tumours in mouse limb and respiratory muscle.
Effectiveness of Lumbopelvic Exercise in Colon Cancer Survivors: A Randomized Controlled Clinical Trial
Pharmacological targeting of mitochondrial function and reactive oxygen species production prevents colon 26 cancer-induced cardiorespiratory muscle weakness
Exercise improves functional capacity and lean body mass in patients with gastrointestinal cancer during chemotherapy: a single-blind RCT
Mitochondrial respiration and H2 O2 emission in saponin-permeabilized murine diaphragm fibers: optimization of fiber separation and comparison to limb muscle
Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation
Evolution of Physical Status From Diagnosis to the End of First-Line Treatment in Breast, Lung, and Colorectal Cancer Patients: The PROTECT-01 Cohort Study Protocol
Increased tumour burden alters skeletal muscle properties in the KPC mouse model of pancreatic cancer.
Imbalanced Subthreshold Currents Following Sepsis and Chemotherapy: A Shared Mechanism Offering a New Therapeutic Target?
FoxP1 is a transcriptional repressor associated with cancer cachexia that induces skeletal muscle wasting and weakness.
Phenotypic features of cancer cachexia-related loss of skeletal muscle mass and function: lessons from human and animal studies.
Muscle-specific deletion of the vitamin D receptor in mice is associated with diaphragm muscle weakness.
Skeletal muscle-specific calpastatin overexpression mitigates muscle weakness in aging and extends life span.
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.