Protein Kinase G I and Heart Failure

Protein Kinase G I and Heart Failure 1269 cardiovascular system has arisen from identifying the different LZ-dependent interacting proteins and kinase substrates of PKGI and PKGI. PKGI and PKGI are each highly expressed in various cardiovascular tissues, including vascular smooth muscle cells (VSMC), cardiac and vascular fibroblasts, endothelium, and CMs. Many prior studies of PKGI focused on understanding its mechanism of inducing VSMC relaxation and arterial dilation. These studies have been reviewed extensively. 1 Whole-body PKGI knockout (KO) leads to abnormal vascular relaxation. And, selective mutation of the PKGI LZ interaction domain in mice also produces hypertension and vascular dysfunction. To date, multiple PKGI and PKGI LZ-dependent substrates have been identified in VSMC, 1 further supporting a critical role of the specific PKGI and PKGI LZ domains in regulating cardiovascular function.