With age, humans tend to lose skeletal muscle mass and its correct functioning. The term for this is sarcopenia which can pose a threat to our life quality and overall freedom. Hence, it helps to better understand sarcopenia and develop therapeutic interventions for slowing, reversing, or preventing its progression.
Also, after the myostatin discovery, a strong negative growth regulator enriched in the skeletal muscle, the medical fraternity developed an interest in it as a probable sarcopenia mediator and therapeutic target. Myostatin, with its complex biology and myostatin inhibition, seems to be a helpful way to address sarcopenia. However, it does face a few challenges. To know more on this topic, you can visit Shenandoah Biotech.
The signaling of myostatin in the skeletal muscle
Myostatin gets considered as a conserved entity that belongs to the superfamily of transforming growth factor- β. And you will find it in vast amounts in the skeletal muscle. It is in lesser concentration in the cardiac muscle and the adipose tissue. Additionally, it gets signaled through the IIB receptor, which gets universally expressed. It also gets formed into a heterodimer along with the kinase four or ALK5. Here the five phosphorylates Smad2 and 3, and the intracellular threonine/serine kinase group of the ALK4 gets complex with the Smad4. And this particular complex then gets translocated to the nucleus for regulating the gene transcription included in the differentiation and proliferation of the skeletal muscle precursor cells and the protein pathways present in the mature myofibers.
The role of myostatin in disease and aging
The human body changes with age. The impact of age on the activity or abundance of the myostatin still needs to be clear. An earlier study done on older, younger, and middle-aged men and womenkind’s that the serum myostatin levels grow with age. It is usually more or “highest” in the older women who are physically frail and is also inversely related to the skeletal muscle mass. Many reports failed to highlight the age-associated difference in circulating the myostatin-immunoreactivity protein or the mRNA levels in the skeletal muscle myostatin. Such disparate findings only suggest that myostatin might not be the primary driver for sarcopenia. On the contrary, it can showcase the complications associated with myostatin and its evaluation.
The use of myostatin inhibition in sarcopenia as a therapy
Since the time it got discovered, there have been many strategies for disrupting myostatin activity, which comprises interacting proteins, neutralizing antibodies, soluble ActRIIB receptors, and properties. Even though myostatin activity and expression changes regarding aging are not well understood, much of its traits make it a desirable and unique target for sarcopenia. The postnatal myostatin inhibition can explicitly increase the muscle mass in older mammals and adults. It has been seen that the weekly injections for neutralizing an antibody to myostatin for about four weeks can dramatically maximize the weight of muscles in an aged mouse by 17%. It also showed improved indices of whole-body metabolism and muscle performance. And in humans, the single dose increased the entire lean mass of the body in postmenopausal women.
