Although several therapeutic agents are currently in development for the treatment of muscle wasting or cachexia in cancer, the majority of these agents do not directly inhibit muscle loss.
A recent study suggests a novel role for parathyroid hormone and its receptor in muscle wasting and cachexia occurring in advanced chronic kidney disease.
Studying how this balance is maintained normally and how it is disrupted in disease conditions will be crucial for understanding and developing treatment regimes for skeletal muscle cachexia.
However, excessive protein degradation in skeletal muscle, and the ensuing muscle loss (cachexia), is highly detrimental for the economy of the human body and can lead to death.
This raises a new perspective for muscle wasting in cancer cachexia whereby degradation could be accelerated through disruption of sarcomeric integrity.
Several animal models for cachexia have shown that TNFα is one of the main cytokines that triggers muscle wasting.
According to group classification, the identified genes provide molecular counterparts of muscle cachexia responsible for actin cytoskeleton rearrangement, actin filament disruption, extracellular matrix dysregulation, protein degradation, energy expenditure, tissue hypoxia, immediate early response, and acute-phase response.
The agreed diagnostic criterion for cachexia was weight loss greater than 5%, or weight loss greater than 2% in individuals already showing depletion according to current bodyweight and height (body-mass index [BMI] <20 kg/m2) or skeletal muscle mass (sarcopenia).
Few studies have addressed the interactions between inflammatory cells and skeletal muscle in cachexia.
These co-morbidities include skeletal muscle wasting (cachexia), cardiovascular disease, lung cancer, osteoporosis and diabetes [ 9].
