Immunoregulatory effects of homocysteine on cardiovascular diseases

Abstract

Hyperhomocysteinemia (HHcy) has been recognized as an independent risk factor for atherosclerosis for more than 30 years, but the mechanisms by which HHcy leads to atherosclerosis are not well fully understood. In this review, we will summarize the immunoregulatory effects of homocysteine on cardiovascular diseases from humoral immunity, monocyte/macrophage and T lymphocyte activity. Homocysteine can induce chemokine and cytokine secretion in monocytes and T lymphocytes and also directly stimulate B lymphocyte proliferation and IgG secretion. In addition, the cellular mechanisms that may explain the pro-inflammatory effect of HHcy are included. Homocysteine may directly or indirectly lead to oxidative stress or endoplasmic reticulum (ER) stress. Elevated levels of homocysteine also decrease the bioavailability of nitric oxide and modulate the levels of other metabolites including S-adenosyl methionine and S-adenosyl homocysteine which may result in cardiovascular diseases.