IRE1α inhibits myostatin through the RIDD pathway to promote skeletal muscle regeneration and repair
IRE1α inhibits myostatin through the RIDD pathway to promote skeletal muscle regeneration and repair
It is understood that in eukaryotic cells, when the endoplasmic reticulum is difficult to bear the unfolded protein load or the metabolism is abnormal, it will cause endoplasmic reticulum stress and activate three classic unfolded protein response (UPR, Unfolded Protein Response) pathways.
At the same time, IRE1 endonuclease can directly degrade specific mRNA substrates through a process called RIDD (regulated IRE1-dependent decay), thereby participating in the regulation of cell survival and function
In order to analyze the mechanism relationship between the IRE1α pathway and the regulation of skeletal muscle function, a mouse model of acute muscle injury induced by cardiotoxin (CTX) found that IRE1α is highly activated in the process of injury-induced muscle regeneration, and is specific to skeletal muscle.
Further molecular mechanism studies have found that during muscle cell differentiation and growth, IRE1α uses the RIDD activity of its endonuclease to degrade myostatin mRNA
In addition, IRE1α, a regulatory mechanism through RIDD activity, is closely related to the progression of muscle wasting disease
This study reveals the key role of IRE1α in the process of muscle regeneration, and clarifies the regulation mode of the IRE1α-Myostatin signal axis in the process of muscle cell differentiation and regeneration, and provides a new potential target for the development of drugs for the treatment of muscle degenerative diseases.
Related paper information: https://doi.
Related paper information: https://doi.
org/10.
1172/JCI143737 https://doi.
org/10.
1172/JCI143737
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