Vascular homeostasis in atherosclerosis: A holistic overview

Figures

• 

  Figure 1. Hallmark of atherosclerosis. (A) The pathogenesis of atherosclerosis. Vascular components of atherosclerotic artery which include tunica adiposa, tunica adventitia, tunica media, sub-endothelium space and tunica intima. For simplicity, external elastic lamina in the blood vessel was not depicted. The interplay of different vascular cell types within the local vascular niche drives atherosclerosis development. Both “inside-out” and “outside-in” mechanism contribute to the development of atherosclerosis. (B) A holistic overview of hallmarks of atherosclerosis and crosstalk among vascular cell components. Atherosclerosis is complex disease involving different cell types at different vascular layers. The hallmark events in different cell types act in concert to promote atheroprogression. CHIP, clonal hematopoiesis of indeterminate potential; ECs, endothelial cells; ECM, extracellular matrix; EndoMT, endothelial-mesenchymal transition; ROS, reactive oxygen species; VSMC, vascular smooth muscle cells.

• 

  Figure 2. Evolving hypothesis of atherosclerosis and vascular homeostasis-targeted therapies. (A) Evolving hypothesis of atherosclerosis. (B) Pharmacological and non-pharmacological strategies to promote vascular stabilization and homeostasis and to prevent atherosclerosis. ACEI, angiotensin-converting-enzyme inhibitors; ARB, angiotensin II receptor blockers; SGLT2i, sodium-glucose cotransporter 2 inhibitor; GLP-1 RA, glucagon-like peptide 1 receptor agonist; KLF2, kruppel-like factor 2.