Defective BVES-mediated feedback control of cAMP in muscular dystrophy.

ABSTRACT: Biological processes incorporate feedback mechanisms to enable positive and/or negative regulation. cAMP is an important second messenger involved in many aspects of muscle biology. However, the feedback mechanisms for the cAMP signaling control in skeletal muscle are largely unknown. Here we show that blood vessel epicardial substance (BVES) is a negative regulator of adenylyl cyclase 9 (ADCY9)-mediated cAMP signaling involved in maintaining muscle mass and function. BVES deletion in mice reduces muscle mass and impairs muscle performance, whereas virally delivered BVES expressed in Bves-deficient skeletal muscle reverses these defects. BVES interacts with and negatively regulates ADCY9's activity. Disruption of BVES-mediated control of cAMP signaling leads to an increased protein kinase

SUBMITTER: Li H 

PROVIDER: S-EPMC10063672 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature