Regulation of cardiovascular calcification by lipids and lipoproteins

Abstract

Purpose of reviewLipids and lipoproteins have long been known to contribute to atherosclerosis and cardiovascular calcification. One theme of recent work is the study of lipoprotein (a) [Lp(a)], a lipoprotein particle similar to LDL-cholesterol that carries a long apoprotein tail and most of the circulating oxidized phospholipids.Recent findingsIn-vitro studies show that Lp(a) stimulates osteoblastic differentiation and mineralization of vascular smooth muscle cells, while the association of Lp(a) with coronary artery calcification continues to have varying results, possibly because of the widely varying threshold levels of Lp(a) chosen for association analyses. Another emerging area in the field of cardiovascular calcification is pathological endothelial-to-mesenchymal transition (EndMT), the process whereby endothelial cell transition into multipotent mesenchymal cells, some of which differentiate into osteochondrogenic cells and mineralize. The effects of lipids and lipoproteins on EndMT suggest that they modulate cardiovascular calcification through multiple mechanisms. There are also emerging trends in imaging of calcific vasculopathy, including: intravascular optical coherence tomography for quantifying plaque characteristics, PET with a radiolabeled NaF tracer, with either CT or MRI to detect coronary plaque vulnerability.SummaryRecent work in this field includes studies of Lp(a), EndMT, and new imaging techniques.

Correlation Analysis of Blood Lipid Level and Thyroid Tumors

“…With the in-depth study of lipid metabolism, it is found that lipid metabolism not only plays a key role in the occurrence and development of cardiovascular diseases, metabolic syndrome and other chronic diseases 11 , but also has a signi cant impact on the occurrence and development of malignant tumors 12 .…”

Associations Between Resolvin D1 and Culprit Plaque Morphologies: An Optical Coherence Tomography Study in Patients with ST-Segment Elevation Myocardial Infarction

“… 1 , 25 However, accumulating evidence suggests that hyperlipidemia and inflammation are actively involved in the pathogenesis of coronary calcification. 30 , 31 Previous studies show that ox-LDL and lp(a) could induce osteoblastic differentiation and mineralization of vascular smooth muscle cells by upregulating expressions of BMP-2, 32 while proinflammatory cytokines (eg, tumor necrosis factor α [TNF-α], interleukin 6 [IL-6], and IL-1β) actively involved in atherosclerosis can also promote matrix mineralization in extraosseous cells. 30 Histological studies show that coronary calcifications usually colocalize with apoptotic macrophages, cholesterol crystals, and large necrotic core within advanced coronary plaques, 1 suggesting that calcifications might be an indicator for unresolved inflammation within the coronary plaques, while associations between RvD1 and culprit plaque calcification could be secondary to chronic local arterial inflammation.…”