Adcy9, also known as adenylate cyclase 9, is an enzyme that produces cyclic-adenosinemonophosphate (cAMP), an important mediator involved in bronchodilation and immunomodulatory response [4]. It is also involved in endothelial signalling pathways relevant to atherogenesis [2].

In mouse models, Adcy9 inactivation improved cardiac function, reduced pathologic remodelling and infarct size after myocardial infarction, accompanied by preserved myocardial capillary density and increased adaptive immune response, with most benefits seen in the absence of CETP [1]. Adcy9 inactivation also protected against atherosclerosis only in the absence of CETP activity, potentially due to decreased macrophage accumulation and proliferation in the arterial wall, improved endothelial function and autonomic tone [3]. In endothelial cells, Adcy9 inactivation increased cAMP accumulation, regulated endothelial permeability and actin cytoskeleton [2].

In conclusion, Adcy9 plays a crucial role in cardiovascular-related biological processes. Gene-inactivation mouse models have revealed its significance in myocardial infarction and atherosclerosis, suggesting that targeting Adcy9 could potentially be a therapeutic strategy for these diseases. Additionally, in asthma, the rs2601796 variant in Adcy9 was associated with severe asthma and less bronchodilator response, highlighting its role in respiratory diseases as well [4].