Доступ предоставлен для: Guest
Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Eukaryotic Gene Expression
Импакт фактор: 2.156 5-летний Импакт фактор: 2.255 SJR: 0.649 SNIP: 0.599 CiteScore™: 3

ISSN Печать: 1045-4403
ISSN Онлайн: 2162-6502

Том 30, 2020 Том 29, 2019 Том 28, 2018 Том 27, 2017 Том 26, 2016 Том 25, 2015 Том 24, 2014 Том 23, 2013 Том 22, 2012 Том 21, 2011 Том 20, 2010 Том 19, 2009 Том 18, 2008 Том 17, 2007 Том 16, 2006 Том 15, 2005 Том 14, 2004 Том 13, 2003 Том 12, 2002 Том 11, 2001 Том 10, 2000 Том 9, 1999 Том 8, 1998 Том 7, 1997 Том 6, 1996 Том 5, 1995 Том 4, 1994

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v10.i2.40
8 pages

Regulatory Mechanisms in Vascular Calcification

Kristina Bostrom
Division of Cardiology, Departments of Medicine and Physiology, UCLA School of Medicine, Los Angeles, CA 90095-1679
Linda L. Demer
Division of Cardiology, Departments of Medicine and Physiology, UCLA School of Medicine, Los Angeles, CA 90095-1679

Краткое описание

Vascular calcification is increasingly recognized as a significant contributor to cardiovascular morbidity and mortality as well as a biologically regulated process potentially subject to prevention and reversal.
Both coronary and aortic calcification are common and influence plaque rupture, angioplasty and surgical complications, and compensatory enlargement. Aortic calcification increases aortic rigidity and contributes to cadiac ischemia, left ventricular hypertrophy, heart failure, and stroke. Calcification is also common in aortic valve leaflets further compounding adverse hemodynamic effects.
Vascular calcification has often been attributed to "passive" crystallization. However, functional similarities between atherosclerotic lesions and bone contradict this view and indicate that it is no more "passive" than in embryonic bone formation or bone repair. Similarities include presence of all the major components of bone osteoid, bone regulatory factors, and subpopulations of artery wall cells that retain osteoblastic lineage potential.
Several animal models for vascular calcification are available. Spontaneous vascular calcification occurs in null mice for matrix GLA protein (MGP), a small matrix protein of unknown function, and osteoprotegerin (OPG), known to modulate osteoclast differentiation. Vascular calcification may also be induced by feeding vitamin D and calcium or warfarin to normal animals, or by fat-feeding mice null for apoE or the LDL-receptor.
Overall, regulation of vascular calcification is a growing field with surprising mechanisms and connections to other fields of biology.

Articles with similar content:

The Role of Gla Proteins in Vascular Calcification
Critical Reviews™ in Eukaryotic Gene Expression, Vol.8, 1998, issue 3-4
Afshin Farzaneh-Far , Diane Proudfoot, Catherine M. Shanahan, Peter L. Weissberg
Matrix Gla-Protein and Its Role in Vascular Calcification
International Journal of Physiology and Pathophysiology, Vol.3, 2012, issue 1
Victoria Yu. Garbuzova, Oleksandr V. Ataman
Chemokines in Respiratory Viral Infections: Focus on Their Diagnostic and Therapeutic Potential
Critical Reviews™ in Immunology, Vol.31, 2011, issue 4
Stavros Apostolakis, Demetrios A. Spandidos, Virginia Amanatidou, Apostolos Zaravinos
Mechanoregulation of Aortic Valvular Interstitial Cell Life and Death
Journal of Long-Term Effects of Medical Implants, Vol.25, 2015, issue 1-2
Kristen L. Billiar, Heather A. Cirka, Mehmet H. Kural
MAIT Cells in COVID-19: Heroes, Villains, or Both?
Critical Reviews™ in Immunology, Vol.40, 2020, issue 2
S. M. Mansour Haeryfar