Inhibition of Myostatin accelerates bone regeneration

[Deleted member 1973]

Inhibition of GDF8 (Myostatin) accelerates bone regeneration in diabetes mellitus type 2

Metabolic diseases like diabetes mellitus cause bone healing deficiencies. We found significant impairment of bone regeneration, osteogenic differentiation and proliferation in diabetic bone. Moreover recent studies suggest a highly underestimated importance of GDF8 (Myostatin) in bone...

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Inhibition of GDF8 (Myostatin) accelerates bone regeneration in diabetes mellitus type 2


Abstract
Metabolic diseases like diabetes mellitus cause bone healing deficiencies. We found significant impairment of bone regeneration, osteogenic differentiation and proliferation in a diabetic bone. Moreover, recent studies suggest a highly underestimated importance of GDF8 (Myostatin) in bone metabolism. Our goal was to analyze the role of GDF8 as a regulator of osteogenic differentiation, proliferation and bone regeneration. We used a murine tibial defect model in diabetic (Leprdb−/−) mice. Myostatin-Inhibitor Follistatin was administered in tibial bony defects of diabetic mice. By means of histology, immunohistochemistry and QRT-PC osteogenesis, differentiation and proliferation were analyzed. Application of Myostatin-inhibitor showed a significant improvement in diabetic bone regeneration compared to the control group (6.5 fold, p < 0.001). Immunohistochemistry revealed a significantly higher proliferation (7.7 fold, p = 0.009), osteogenic differentiation (Runx-2: 3.7 fold, p = 0.011, ALP: 9.3 fold, p < 0.001) and calcification (4.9 fold, p = 0.024) in Follistatin treated diabetic animals. Therapeutical application of Follistatin, known for the importance of muscle diseases, plays an important role in bone metabolism. Diabetic bone revealed an overexpression of the catabolic protein Myostatin. Antagonization of Myostatin in diabetic animals leads to a restoration of impaired bone regeneration and represents a promising therapeutic option.
Introduction
Bone regeneration is usually an efficient process without scarring. However, diseases such as diabetes mellitus can cause higher fracture rates accompanied by non-unions and a detrimentally diminished healing capacity1,2,3. In 2013, 382 million people were suffering from diabetes mellitus worldwide with a predicted increase to 592 million in 2035, thus diabetes appears to be the most common and epidemiologically most relevant endocrinological disease4. Summarized, the economic impact of diabetes-associated bone healing impairment and current insufficient therapeutics lead to a high demand in developing novel treatment strategies.



The heart is muscle as well and we definitely don't want it to get bigger.

The heart does produce less myostatin than other muscle but it does produce it and by inhibiting myostatin activity it is quite possible that the heart would grow as well,

and this would be really bad.

It is quite possible that by inhibiting myostatin you will have heart problems later in life and it will also hurt your gains as well,

so I think that myostatin inhibitors are pointless

but they might be useful in the future when scientists discover selective myostatin inhibitors that work only on skeletal muscle tissues.


the biggest issue with myostatin inhibitors is that it would cause all muscles to grow, including cardiac and smooth muscle and we don't want them to grow. ​

 

[Deleted member 1973]

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[GTFIH]!!!