Abstract
Phosphatidylinositol 3 kinase (PI3K) is a key molecule in the initiation of signal transduction pathways after the binding of extracellular signals to cell surface receptors. An intracellular kinase, PI3K activates multiple intracellular signaling pathways that affect cell growth, proliferation, migration, secretion, differentiation, transcription and translation. Dysregulation of PI3K activity, and as aberrant PI3K signaling, lead to a broad range of human diseases, such as cancer, immune disorders, diabetes, and cardiovascular diseases. A growing number of studies have shown that PI3K and its signaling pathways play key roles in the pathophysiological process of atherosclerosis. Furthermore, drugs targeting PI3K and its related signaling pathways are promising treatments for atherosclerosis. Therefore, we have reviewed how PI3K, an important regulatory factor, mediates the development of atherosclerosis and how targeting PI3K can be used to prevent and treat atherosclerosis.
Highlights
Atherosclerosis is a leading cause of vascular death worldwide (Herrington et al, 2016)
We used sufficient experimental evidence to demonstrate that the advanced glycation end-product Nε-carboxymethyl-lysine (CML) promotes foam cell apoptosis (Figure 2) in diabetic atherosclerotic plaques through classic apoptosis pathways (Bcl-2/Bax, caspase-3 and caspase-9) in a concentrationdependent manner, and we suggested that the underlying mechanism involved inhibition of the Phosphatidylinositol 3 kinase (PI3K)/Akt signaling pathways (Wang et al, 2019)
Effect Regulate autophagy to reduce oxidative stress Reduce ischemia/reperfusion injury Promote ischemic disease-induced angiogenesis protein 27 increases the expression of ATP-binding cassette transporter A1 (ABCA1), promoting the outflow of macrophage cholesterol, reducing the accumulation of cholesterol in macrophages, and preventing the development of foam cells and macrophages to reduce the formation of atherosclerotic plaques (Kuang et al, 2017)
Summary
Atherosclerosis is a leading cause of vascular death worldwide (Herrington et al, 2016). Activation of PI3K/Akt signaling can induce monocyte chemotaxis, macrophage migration, increased intracellular lipid accumulation, neovascularization, SMC proliferation and dysfunction in lesions, all of which are involved in plaque formation.
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