id	author	title	date	pages	extension	mime	words	sentence	flesch	summary	cache	txt
ajlm-2582	Jadali, Zohreh	Pathobiology of HIV-related metabolic and cardiovascular comorbidities: Towards a unifying mechanism	2024		.htm	text/html	1348	56	28	This is supported by elevation of intermediate/inflammatory monocytes with proatherogenic properties in HIV-positive patients.5 These cells play a detrimental role in CVD progression and can express abundant tissue factor, a risk marker for CVDs.5 Lipidic environment modification is another reason for production of tissue factor in plaque macrophages; thus, interplay of lipids and immune cells might in part be responsible for the CVD progression in infected patients.5 Elevation of macrophage activation markers, soluble CD14, in HIV-positive patients provides additional evidence for the importance of the monocyte-macrophage lineage, because they can be associated with clinical CVD events and dyslipidaemia.6 Monocyte and macrophage dysfunction in cholesterol handling as a cause of HIV infection may also affect the CVD risk.5 This may occur by down-regulation of adenosine triphosphate-binding cassette transporter A1, which is essential for cholesterol homeostasis and high-density lipoprotein metabolism.5 Dysregulated inflammation is another risk factor for both CVD and dyslipidaemia in HIV-positive patients.7 This is supported by evidence, including (1) the increased level of high-sensitivity C-reactive protein as a nonspecific inflammatory marker that increases the CVD risk and dyslipidaemia, (2) the increased levels of D-dimer that can indicate a positive association with lipid indicators in patients with coronary artery disease, and (3) the increased production of interleukin-6 that occurs during HIV replication and is associated with dyslipidaemia and increased CVD risk.7 Loss of gut barrier function and the ensuing microbial translocation that is usually associated with HIV disease progression can also elicit an inflammatory cascade.8 This inflammatory response may induce CVD through alteration in the balance of T-helper 17/regulatory T-cells and their associated cytokines.9 T-helper 17/regulatory T-cells appear to be a bridge linking the gut microbiota to host metabolic disorders.9 T-helper 17 and regulatory T-cells have antagonistic effects. These clinical conditions are strongly influenced by both elements of the immune system and a broad group of lipid components.4 HIV-positive individuals also have elevated proportions of T-helper 17 cells, which may promote inflammation, and senescent cells, which may increase risk of cardiovascular disease, in hyperlipidemic conditions.4 Interleukin-2 production has also been shown to increase in these patients and can affect lipid metabolism and CVD risk.4 Cells of the monocyte-macrophage lineage appear to also play a role in the complicated connection between the immune system and HIV disease, dyslipidaemia, and CVDs.5	cache/ajlm-2582.htm	txt/ajlm-2582.txt