The DOI matches its Crossref record; 136 of the 136 references it cites were found in a registry or an index.
Vascular Calcification: The Killer of Patients with Chronic Kidney Disease
Abstract
Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Vascular calcification is a common complication in CKD, and investigators have demonstrated that the extent and histoanatomic type of vascular calcification are predictors of subsequent vascular mortality. Although research efforts in the past decade have greatly improved our knowledge of the multiple factors and mechanisms involved in vascular calcification in patients with kidney disease, many questions remain unanswered. No longer can we accept the concept that vascular calcification in CKD is a passive process resulting from an elevated calcium-phosphate product. Rather, as a result of the metabolic insults of diabetes, dyslipidemia, oxidative stress, uremia, and hyperphosphatemia, "osteoblast-like" cells form in the vessel wall. These mineralizing cells as well as the recruitment of undifferentiated progenitors to the osteochondrocyte lineage play a critical role in the calcification process. Important transcription factors such as Msx 2, osterix, and RUNX2 are crucial in the programming of osteogenesis. Thus, the simultaneous increase in arterial osteochondrocytic programs and reduction in active cellular defense mechanisms creates the "perfect storm" of vascular calcification seen in ESRD. Innovative clinical studies addressing the combined use of inhibitors that work on vascular calcification through distinct molecular mechanisms, such as fetuin-A, osteopontin, and bone morphogenic protein 7, among others, will be necessary to reduce significantly the accrual of vascular calcifications and cardiovascular mortality in kidney disease. In addition, the roles of oxidative stress and inflammation on the fate of smooth muscle vascular cells and their function deserve further translational investigation.
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Cites
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Cited by
Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease
Hu, M. C., Shi, M., Zhang, J., Quiñones, H., Griffith, C., Kuro-o, M., & Moe, O. W. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2009121311 · Cited by 926
Cause of Death in Patients with Reduced Kidney Function
Thompson, S., James, M., Wiebe, N., Hemmelgarn, B., Manns, B., Klarenbach, S., & Tonelli, M. (2015) · Journal of the American Society of Nephrology · doi:10.1681/asn.2014070714 · Cited by 658
Hu, M. C., Shiizaki, K., Kuro-o, M., & Moe, O. W. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183727 · Cited by 587
Vitamin D, disease and therapeutic opportunities
Plum, L. A., & DeLuca, H. F. (2010) · Nature Reviews Drug Discovery · doi:10.1038/nrd3318 · Cited by 477
AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms
He, L., Wei, Q., Liu, J., Yi, M., Liu, Y., Liu, H., Sun, L., Peng, Y., Liu, F., Venkatachalam, M. A., et al. (2017) · Kidney International · doi:10.1016/j.kint.2017.06.030 · Cited by 448
Metadata
- Authors
- Mizobuchi, M., Towler, D., & Slatopolsky, E.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2009-07
- Volume
- 20
- Issue
- 7
- Pages
- 1453-1464
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2146662079
- Cited by
- 542
- References
- 136
- FWCI
- 19.38
- Type
- journal article
- Language
- en
- Open access
- closed
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