-
the prodomain:GDF8 complex can exist in a fully latent state and an activated or "triggered" state where the prodomain remains in complex with the mature domain
-
Myostatin deletion increases lean muscle mass and results in muscle-specific increases in endothelium-dependent vasodilation.
-
Indoxyl sulfate enhanced the production of myostatin by enhancing oxidative stress in skeletal muscle, leading to muscle atrophy.
-
Myostatin inhibition therapy for insulin-deficient type 1 diabetes has been proposed in an experimental model.
-
maternal myostatin deficiency altered fetal growth and calvarial collagen content of newborn mice and conferred a lasting impact on bone geometry and biomechanical integrity of offspring at 4 mo of age.
-
Mstn regulates Fndc5/Irisin expression and secretion through a novel miR-34a-dependent post-transcriptional mechanism; loss of Mstn in mice leads to the increased Fndc5/Irisin expression, which contributes to the browning of white adipocytes
-
Axon diameter and myelin thickness were increased in motor axons of myostatin deficient animals.
-
These data illustrate the importance of lipids as a link by which MSTN deficiency can impact mitochondrial bioenergetics in skeletal muscle.
-
Myostatin inhibits eEF2K-eEF2 by regulating AMPK to suppress protein synthesis.
-
These results demonstrate that a greater than additive effect is observed on the growth of skeletal muscle and in the reduction of body fat when myostatin is absent and IGF1 is in excess, and that myostatin and IGF1 regulate skeletal muscle size, myofibre type and gonadal fat through distinct mechanisms.
-
Mstn deficiency but not anti-myostatin blockade induces marked proteomic changes in mouse skeletal muscle.
-
GDF8 plays a significant regulatory role in bone formation and bone resorption
-
Genetic inactivation of myostatin increases maximal force and power, but in return it reduces muscle quality, particularly in male mice.
-
findings indicate that myostatin directly influences osteocyte function and thereby inhibits osteoblastic differentiation, at least in part, through the suppression of osteocyte-derived exosomal miR-218, suggesting a novel mechanism in muscle-bone communication.
-
The 12-bp Mstn(Cmpt-dl1Abc) deletion decreases adiposity and improves whole body glucose uptake, insulin sensitivity, and (18)FDG uptake of skeletal muscle and white adipose tissue.
-
In this model, increased LTBP4 led to greater muscle mass with proportionally increased strength, and decreased fibrosis. The increase in muscle mass and reduction in fibrosis were similar to what occurs when myostatin, a related TGFbeta family member and negative regulator of muscle mass, was deleted in mdx mice
-
myostatin dysfunction impairs adaptation of the soleus muscle to high functional demands.
-
Evidences indicate that the suppression of MSTN cause to increase the regenerative potential of injured soleus muscle via the increase in the population of muscle satellite cells regardless of unloading conditions.
-
A role for Nfix in postnatal skeletal muscle development and regeneration and Myostatin gene expression regulation.
-
Myostatin deletion specifically affects skeletal muscle mitochondrial function and redox status. Decreased mitochondrial function and oxidative markers persisted in aged mstn KO mice. However, muscle hypertrophy and the redox status related to this genotype appeared as beneficial side effects attenuating the age effect, as metabolic changes become less pronounced in comparison with WT mice.
