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Immunoregulatory effects of homocysteine on cardiovascular diseases
1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100083, China.
Insights
Hyperhomocysteinemia (HHcy) promotes atherosclerosis by triggering immune responses and cellular stress. Understanding homocysteine
Area of Science:
- Immunology
- Cardiovascular Science
- Biochemistry
Background:
- Hyperhomocysteinemia (HHcy) is a known risk factor for atherosclerosis.
- Mechanisms linking HHcy to atherosclerosis remain incompletely understood.
Purpose of the Study:
- To review the immunoregulatory effects of homocysteine on cardiovascular diseases.
- To elucidate cellular mechanisms underlying HHcy's pro-inflammatory impact.
Main Methods:
- Review of existing literature on homocysteine's effects on immune cells.
- Analysis of cellular pathways including oxidative and ER stress.
Main Results:
- Homocysteine influences humoral immunity, monocyte/macrophage, and T lymphocyte activity.
- It induces chemokine/cytokine secretion and stimulates B lymphocyte proliferation and IgG secretion.
- HHcy contributes to oxidative stress, ER stress, and reduced nitric oxide bioavailability.
Conclusions:
- HHcy exerts pro-inflammatory effects on the cardiovascular system through immune modulation and cellular stress.
- Understanding these mechanisms is crucial for developing therapeutic strategies against HHcy-related 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.
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