Trained immunity in monocyte/macrophage: Novel mechanism of phytochemicals in the treatment of atherosclerotic cardiovascular disease

Front Pharmacol. 2023 Feb 21:14:1109576. doi: 10.3389/fphar.2023.1109576. eCollection 2023.

Abstract

Atherosclerosis (AS) is the pathology of atherosclerotic cardiovascular diseases (ASCVD), characterized by persistent chronic inflammation in the vessel wall, in which monocytes/macrophages play a key role. It has been reported that innate immune system cells can assume a persistent proinflammatory state after short stimulation with endogenous atherogenic stimuli. The pathogenesis of AS can be influenced by this persistent hyperactivation of the innate immune system, which is termed trained immunity. Trained immunity has also been implicated as a key pathological mechanism, leading to persistent chronic inflammation in AS. Trained immunity is mediated via epigenetic and metabolic reprogramming and occurs in mature innate immune cells and their bone marrow progenitors. Natural products are promising candidates for novel pharmacological agents that can be used to prevent or treat cardiovascular diseases (CVD). A variety of natural products and agents exhibiting antiatherosclerotic abilities have been reported to potentially interfere with the pharmacological targets of trained immunity. This review describes in as much detail as possible the mechanisms involved in trained immunity and how phytochemicals of this process inhibit AS by affecting trained monocytes/macrophages.

Keywords: atherosclerosis; epigenetic reprogramming; metabolic reprogramming; monocyte/macrophage; natural products; trained immunity.

Publication types

  • Review

Grants and funding

This work was supported by grants from the Programs Foundation for Leading Talents in National Administration of Traditional Chinese Medicine of China “Qihuang scholars” Project (no. 0201000401), the National Natural Science Foundation of China (no. 81974556), and the National Key Research and Development Program of China (no. 2020YFC2002701).