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Recent advances in our understanding of the biology of muscle, and how anabolic and catabolic stimuli interact to control muscle mass and function, have led to new interest in the pharmacological treatment of muscle wasting. Loss of muscle occurs as a consequence of several chronic diseases cachexia as well as normal aging sarcopenia.
Sarcopenic and cachectic muscles have been demonstrated to be abundant in myostatin- and apoptosis-linked molecules. The ubiquitinβproteasome system UPS is activated during many different types of cachexia cancer cachexia, cardiac heart failure, chronic obstructive pulmonary disease , but not many mediators of the UPS change during sarcopenia. Some studies have indicated a change of autophagic signaling during both sarcopenia and cachexia, but the adaptation remains to be elucidated.
This review provides an overview of the adaptive changes in negative regulators of muscle mass in both sarcopenia and cachexia. Loss of muscle is a serious consequence of many chronic diseases and of aging itself because it leads to weakness, loss of independence, and increased risk of death.
Unfortunately, the field suffers from having more definitions than therapies; muscle wasting is an inevitable part of aging, where it is known as sarcopenia [ 1 ]. Muscle loss is also common in most organ failure diseasesβheart failure, liver or renal failure, chronic obstructive pulmonary disease COPD βand in some types of cancer. In such settings, it is known as cachexia [ 2 ]. Of course, muscle wasting is also inevitable during starvation.
