9th International Science Congress (ISC-2019).  International E-publication: Publish Projects, Dissertation, Theses, Books, Souvenir, Conference Proceeding with ISBN.  International E-Bulletin: Information/News regarding: Academics and Research

A review of obstacles facing reversal of vascular calcification

Author Affiliations

  • 1Department of Biomedical, Industrial and Human Factors Engineering, Wright State University,Dayton, OH 45435 USA
  • 2Department of Biomedical, Industrial and Human Factors Engineering, Wright State University,Dayton, OH 45435 USA

Int. Res. J. Medical Sci., Volume 7, Issue (2), Pages 6-8, May,28 (2019)

Abstract

Cardiovascular disease (CVD) refers to several types of conditions that affect the heart and blood vessels.CVD is the leading cause of death in the world and is often characterized by pathological vascular calcification, which has been recognized as a major risk factor for various cardiovascular events including heart failure, pulmonary hypertension (PTH), and death in chronic kidney disease (CKD) patients. To date, there are no therapies to reverse medial or intimal calcification. In this mini-review we aim to shed light on the relationship between macrophages, osteoclasts, and vascular calcification.

References

  1. Moe S.M. and Chen N.X. (2008)., Mechanisms of vascular calcification in chronic kidney disease., Journal of the American Society of Nephrology, 19(2), 213-216.
  2. Blair H.C. (1998)., How the osteoclast degrades bone., BioEssays : news and reviews in molecular, cellular and developmental biology, 20(10), 837-846. doi:10.1002/(sici)1521-1878(199810)20:10<837::aid-bies9>3.0.co;2-d.
  3. Sato K. and Takayanagi H. (2006)., Osteoclasts, rheumatoid arthritis, and osteoimmunology., Current opinion in rheumatology, 18(4), 419-426. doi:10.1097/01.bor.0000231912.24740.a5.
  4. Doherty T.M., Uzui H., Fitzpatrick L.A., Tripathi P.V., Dunstan C.R., Asotra K. and Rajavashisth T.B. (2002)., Rationale for the role of osteoclast-like cells in arterial calcification., The FASEB journal, 16(6), 577-582.
  5. Boyle W.J., Simonet W.S. and Lacey D.L. (2003)., Osteoclast differentiation and activation., Nature, 423(6937), 337. doi:10.1038/nature01658.
  6. Kong Y.Y., Yoshida H., Sarosi I., Tan H.L., Timms E., Capparelli C. and Khoo W. (1999)., OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis., Nature, 397(6717), 315-323. doi:10.1038/16852.
  7. Stanley E.R., Berg K.L., Einstein D.B., Lee P.S., Pixley F. J., Wang Y. and Yeung Y.G. (1997)., Biology and action of colony‐stimulating factor‐1., Molecular Reproduction and Development: Incorporating Gamete Research, 46(1), 4-10. doi:10.1002/(sici)1098-2795(199701)46:1<4::aid-mrd2>3.0.co;2-v.
  8. Wu M., Rementer C. and Giachelli C.M. (2013)., Vascular calcification: an update on mechanisms and challenges in treatment., Calcified tissue international, 93(4), 365-373. doi:10.1007/s00223-013-9712-z.
  9. Qiao J.H., Tripathi J., Mishra N.K., Cai Y., Tripathi S., Wang X.P. and Lusis A.J. (1997)., Role of macrophage colony-stimulating factor in atherosclerosis: studies of osteopetrotic mice., The American journal of pathology, 150, 1687-1699.
  10. Spicer S.S., Lewis S.E., Tashian R.E. and Schulte B.A. (1989)., Mice carrying a CAR-2 null allele lack carbonic anhydrase II immunohistochemically and show vascular calcification., The American journal of pathology, 134(4), 947-954.
  11. Han K.H., Hennigar R.A. and O'neill W.C. (2015)., The association of bone and osteoclasts with vascular calcification., Vascular Medicine, 20(6), 527-533. doi:10.1177/1358863x15597076.
  12. Sage A.P., Tintut Y. and Demer L.L. (2010)., Regulatory mechanisms in vascular calcification., Nature reviews. Cardiology, 7, 528-536. doi:10.1038/nrcardio.2010.115.
  13. Price P.A., June H.H., Buckley J.R. and Williamson M.K. (2001)., Osteoprotegerin inhibits artery calcification induced by warfarin and by vitamin D., Arteriosclerosis, thrombosis, and vascular biology, 21(10), 1610-1616.
  14. Panizo S., Cardus A., Encinas M., Parisi E., Valcheva P., López-Ongil S. and Valdivielso J.M. (2009)., RANKL increases vascular smooth muscle cell calcification through a RANK-BMP4-dependent pathway., Circulation research, 104(9), 1041-1048.
  15. Deuell K.A., Callegari A., Giachelli C.M., Rosenfeld M.E. and Scatena M. (2012)., RANKL enhances macrophage paracrine pro-calcific activity in high phosphate-treated smooth muscle cells: dependence on IL-6 and TNF-α., Journal of vascular research, 49(6), 510-521. doi:10.1159/000341216.
  16. Lei Y., Iwashita M., Choi J., Aikawa M. and Aikawa E. (2015)., N-acetylglucosamine-1-Phosphate Transferase Suppresses Lysosomal Hydrolases in Dysfunctional Osteoclasts: A Potential Mechanism for Vascular Calcification., Journal of cardiovascular development and disease, 2, 31-47. doi:10.3390/jcdd2020031.
  17. Mozar A., Haren N., Chasseraud M., Louvet L., Mazière C., Wattel A. and Mazière J.C. (2008)., High extracellular inorganic phosphate concentration inhibits RANK-RANKL signaling in osteoclast-like cells., Journal of cellular physiology, 215, 47-54. doi:10.1002/jcp.21283.
  18. Giachelli C.M., Jono S., Shioi A., Nishizawa Y., Mori K. and Morii H. (2001)., Vascular calcification and inorganic phosphate., American journal of kidney diseases, 38(4), S34-S37.