The Role and Mechanisms of Histone Acetyltransferases in Arterial Lesions

Cardiovascular and cerebrovascular diseases are among the leading causes of death worldwide. Development of these diseases occurs following pathological structural remodeling and functional changes in the vascular wall. Emerging evidence suggests that histone acetyltransferases (HATs) play a role in the pathological processes of the arterial wall. However, there is currently a lack of comprehensive reviews examining the role of HATs in vascular diseases. The aim of this research is therefore to systematically describe the pathological effects of various risk factors on different layers of cells in the arterial vascular wall. The risk factors include abnormal activation of the renin-angiotensin system, hyperglycemia, high-sodium diets, and intermittent hypoxia. The effects regulated by HATs involve the nuclear factor kappa-B (NF-κB)-NOD-like receptor family pyrin domain containing 3 (NLRP3) and AMP-activated protein kinase (AMPK) pathways, and the mitogen-activated protein kinase (MAPK) and vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathways. We also explore the dual role of HATs in vascular protection and injury. Additionally, this study focuses on the prospects of future therapeutic strategies targeting HATs, including innovative approaches such as HAT inhibitors, epigenetic degraders, non-coding RNA interventions, and epigenetic editing technologies. The aim of this review is to provide a basis for the development of selective subtype HAT inhibitors.