Vascular calcification is the deposition of calcium phosphate minerals in vascular tissue. Vascular calcification occurs by both active and passive processes. Extent and tissue-specific patterns of vascular calcification are predictors of cardiovascular morbidity and mortality. The placenta is a highly vascularized organ with specialized vasculature that mediates communication between two circulatory systems. At delivery the placenta often contains calcified tissue and calcification can be considered a marker of viral infection, but the mechanisms, histoanatomical specificity, and pathophysiological significance of placental calcification are poorly understood. In this review, we outline the current understanding of vascular calcification mechanisms, biomedical consequences, and therapeutic interventions in the context of histoanatomical types. We summarize available placental calcification data and clinical grading systems for placental calcification. We report on studies that have examined the association between placental calcification and acute adverse maternal and fetal outcomes. We then review the intersection between placental dysfunction and long-term cardiovascular health, including subsequent occurrence of maternal vascular calcification. Possible maternal phenotypes and trigger mechanisms that may predispose for calcification and cardiovascular disease are discussed. We go on to highlight the potential diagnostic value of placental calcification. Finally, we suggest avenues of research to evaluate placental calcification as a research model for investigating the relationship between placental dysfunction and cardiovascular health, as well as a biomarker for placental dysfunction, adverse clinical outcomes, and increased risk of subsequent maternal and offspring cardiovascular events.
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http://dx.doi.org/10.3389/fphys.2018.01044 | DOI Listing |
J Clin Med
December 2024
Division of Plastic, Aesthetic and Reconstructive Surgery, Department of Surgery, Medical University of Graz, 8036 Graz, Austria.
Non-healing soft tissue defects pose challenges to treating physicians. Microsurgical reconstruction is a treatment option for achieving wound closure and limb salvage. These free tissue transfers are often challenging due to associated risk factors.
View Article and Find Full Text PDFNutrients
December 2024
Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou 510080, China.
Background: Atherosclerotic calcification (AC) is a common feature of atherosclerotic cardiovascular disease. β-Hydroxybutyrate (BHB) has been identified as a molecule that influences cardiovascular disease. However, whether BHB can influence AC is still unknown.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Vascular Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: The impact of moderate-to-vigorous physical activity (MVPA) on all-cause mortality in type 2 diabetes (T2D) patients with severe abdominal aortic calcification (SAAC) remains unclear.
Methods: We analyzed data from the National Health and Nutrition Examination Survey (NHANES) 2013-2014, including T2D patients aged 40 years and older. AAC was assessed using the Kauppila scoring system, with SAAC defined as a score >6.
Cardiovasc Res
December 2024
Department of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Aim: Microcalcification increases the vulnerability of plaques and has become an important driver of acute cardiovascular events in diabetic patients. However, the regulatory mechanisms remain unclear. DJ-1, a multifunctional protein, may play a potential role in the development of diabetic complications.
View Article and Find Full Text PDFClin Kidney J
January 2025
MP3CV Laboratory, Jules Verne University of Picardie, Amiens, France.
Background: The serum calcification propensity test (or T50 test) might become a standard tool for the assessment of vascular calcification risk and T50 might be a valuable biomarker in clinical trials of treatments intended to slow the progression of vascular calcification. Literature data suggest that non-calcium-containing phosphate binders can influence T50 in chronic dialysed patients. However, it is not clear whether similar interventions are effective in patients at earlier stages of chronic kidney disease (CKD).
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