Fig. 2: The modulation of effective autophagy and efferocytosis in foam cell/ lipid-laden macrophage by phytochemicals in atherosclerosis plaque.

A The entry of monocytes into the intima. Monocytes migrate from the bloodstream into the innermost layer of the artery wall, called the intima. Once in the intima, the monocytes differentiate into macrophages. B illustrates the formation of foam cells. In intima, macrophages start to accumulate modified lipoproteins, such as oxidized low-density lipoprotein (Ox-LDL), leading to the formation of foam cells. The accumulation of these foam cells, along with other cellular debris and extracellular matrix, leads to the formation of an atherosclerotic plaque within the intima of the artery wall. In this case, this cell can modulate by normal autophagy via phytochemicals. C, D shows the effect of drug-eluting stents containing phytochemicals, leading to an increase in autophagy. E This illustrates that improved autophagy induced by phytochemicals can promote efferocytosis, and conversely, increased efferocytosis can enhance autophagy. Ultimately, this balance fosters an anti-inflammatory environment, reduces atherosclerotic plaque development, and improves plaque stability. Thus, by incorporating phytochemicals, the drug-eluting stents could potentially provide added therapeutic benefits beyond the currently used pharmaceutical drugs, leading to improved long-term outcomes for patients with atherosclerotic cardiovascular disease. Additional details about the intricate factors and pathways connecting autophagy and efferocytosis, along with specific phytochemicals that can regulate this balance, can be found in Table 2.