**10. Summary and conclusions**

The paramount importance of CVD on morbidity and mortality in the United States and globally is clear, yet inefficiencies in the clinical translation of basic science findings show that the underlying mechanisms of CVD are still not completely known and fully effective therapies against CVD are still needed. Indeed, despite ample basic and clinical research, CVD preva‐ lence is estimated to increase 10% and the economic burden of CVD is projected to triple within the next 20 years with latest estimates that >40% of the adult US population will have some form of CVD by the year 2030 [50]. In our incessant search for possible targets to help control and possibly eliminate CVD, the pivotal influence of VSM growth in playing key roles in CVD pathogenesis is clear. We and others have focused our efforts on identifying and characterizing unique elements behind VSM biology and signaling under healthy as well as pathologic conditions, and findings to date reveal significant insights into many biochemical, molecular, and cellular elements foundational to CVD with perhaps that of cyclic nucleotide signaling at the forefront. Given its ubiquitous nature and multifaceted diverse functions, cyclic AMP and cyclic GMP and their downstream kinases and targets including VASP represent key elements capable of controlling deleterious vascular growth that serves as a basis for CVD. Only through persistent basic science and clinical investigation do we hope to fully understand these crucial factors that hold great promise in our seemingly never-ending struggle to combat and control CVD.
