Abstract
The influence of hyperhomocysteinemia (HHCy) on cardiovascular disease (CVD) remains unclear. HHCy is associated with inflammation and atherosclerosis, and it is an independent risk factor for CVD, stroke and myocardial infarction. However, homocysteine (HCy)-lowering therapy does not affect the inflammatory state of CVD patients, and it has little influence on cardiovascular risk. The HCy degradation product hydrogen sulfide (H2S) is a cardioprotector. Previous research proposed a positive role of H2S in the cardiovascular system, and we discuss some recent data suggesting that HHCy worsens CVD by increasing the production of H2S, which decreases the expression of adenosine A2A receptors on the surface of immune and cardiovascular cells to cause inflammation and ischemia, respectively.
Highlights
Cardiovascular disease (CVD) includes conditions that affect the heart or blood vessels.The heart is a pump, and blood vessels are conduits for blood and cells that supply oxygen and nutrients to maintain the molecular mechanisms necessary for vascular development and the functioning of different tissues
It is believed that plaques with a reduced ratio of smooth muscle cells to foam cells are vulnerable to rupture, which is the event inducing thrombosis and, myocardial infarction [1]
The transport of adenosine across the cell membrane is crucial because it regulates the levels of extracellular adenosine that come into contact with surface receptors
Summary
Cardiovascular disease (CVD) includes conditions that affect the heart or blood vessels. The heart is a pump, and blood vessels are conduits for blood and cells that supply oxygen and nutrients to maintain the molecular mechanisms necessary for vascular development and the functioning of different tissues. Each organ has its own capillary network to fulfill its specific functions, and endothelial cells provide the microvasculature of the different organs These endothelial cells form a vascular wall that controls organ development, homeostasis and tissue regeneration. Circulating monocytes adhere to activate endothelial cells, enter the vascular wall, and differentiate into tissue macrophages. These macrophages ingest lipoproteins and turn into foam cells. Of all the established risk factors associated with the development of hypertension and its complications such as accelerated cardiac atherosclerosis and premature death, HHCy is probably the most elusive. HHCy causes an increase in H2 S levels, which affects the adenosinergic system, promoting CVD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
