Interactive and Multifactorial Mechanisms of Calcific Vascular and Valvular Disease

Linda L Demer; Yin Tintut

doi:10.1016/j.tem.2019.06.001

Interactive and Multifactorial Mechanisms of Calcific Vascular and Valvular Disease

Trends Endocrinol Metab. 2019 Sep;30(9):646-657. doi: 10.1016/j.tem.2019.06.001. Epub 2019 Jul 3.

Authors

Linda L Demer¹, Yin Tintut²

Affiliations

¹ Department of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1679, USA; Department of Physiology, University of California at Los Angeles, Los Angeles, CA 90095-1751, USA; Department of Bioengineering, University of California at Los Angeles, Los Angeles, CA 90095-1600, USA. Electronic address: LDemer@mednet.ucla.edu.
² Department of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1679, USA; Department of Physiology, University of California at Los Angeles, Los Angeles, CA 90095-1751, USA; Department of Orthopaedic Surgery, University of California at Los Angeles, Los Angeles, CA 90095, USA.

Abstract

Calcific vascular and valvular disease (CVVD) is widespread and has major health consequences. Although coronary artery calcification has long been associated with hyperlipidemia and increased mortality, recent evidence suggests that its progression is increased in association with cholesterol-lowering HMG-CoA reductase inhibitors ('statins') and long-term, high-intensity exercise. A nationwide trial showed no cardiovascular benefit of vitamin D supplements. Controversy remains as to whether calcium deposits in plaque promote or prevent plaque rupture. CVVD appears to occur through mechanisms similar to those of intramembranous, endochondral, and osteophytic skeletal bone formation. New evidence implicates autotaxin, endothelial-mesenchymal transformation, and microRNA and long non-coding RNA (lncRNA) as novel regulatory factors. New therapeutic options are being developed.

Keywords: atherosclerosis; bone; calcification; cardiovascular; valvular disease.

Publication types

Research Support, N.I.H., Extramural
Review

MeSH terms

Animals
Atherosclerosis / drug therapy
Atherosclerosis / metabolism*
Atherosclerosis / physiopathology
Cardiovascular System / drug effects
Cardiovascular System / metabolism
Heart Valve Diseases / drug therapy
Heart Valve Diseases / metabolism
Heart Valve Diseases / physiopathology
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
Vitamin D / therapeutic use

Substances

Hydroxymethylglutaryl-CoA Reductase Inhibitors
Vitamin D

Abstract

Publication types

MeSH terms

Substances

Grants and funding