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Updated: Nov 23, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
An update on vascular calcification and potential therapeutics
Anubha Singh1, Simran Tandon2, Chanderdeep Tandon3
1Amity Institute of Biotechnology (AIB), Amity University Uttar Pradesh, Noida, Uttar Pradesh, India.
Insights
Pathological calcification, a complex cell-mediated process, significantly contributes to cardiovascular disease, especially in patients with chronic kidney disease. Research explores novel drug targets and interventions to manage and potentially reverse vascular calcification.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Biochemistry
Background:
- Pathological calcification is a primary driver of cardiovascular morbidities, particularly in individuals with chronic kidney disease (CKD), end-stage renal disease (ESRD), and metabolic disorders.
- Vascular calcification is an active, cell-mediated process influenced by metabolic insults like diabetes, hypertension, dyslipidemia, and atherosclerosis, rather than a passive event.
Purpose of the Study:
- To review the intricate relationship between vascular calcification and associated clinical diseases.
- To identify key regulators and genetic factors contributing to pathological calcification.
- To explore novel therapeutic avenues and drug development for preventing and reversing vascular calcification.
Main Methods:
- Literature review focusing on cellular mechanisms of calcification.
- Analysis of various factors inducing vascular calcification, including bone formation, apoptosis, and Ca-P balance.
- Examination of current and emerging interventions targeting calcification.
Main Results:
- Vascular calcification involves complex mechanisms such as induced bone formation, apoptosis, altered calcium-phosphorus balance, and loss of inhibitory factors.
- Numerous interventions are under investigation, including phosphate binders, vitamin K, calcimimetics, vitamin D, bisphosphonates, and TNAP inhibitors.
- Genetic factors have been identified as contributors to pathological calcification.
Conclusions:
- Current preventive measures for pathological calcification are limited.
- Targeting cellular mechanisms offers promising avenues for developing new drugs and treatment strategies.
- Further research is needed to develop effective treatments for reversing or curing pathological calcification.
Abstract:
Pathological calcification is a major cause of cardiovascular morbidities primarily in population with chronic kidney disease (CKD), end stage renal diseases (ERSD) and metabolic disorders. Investigators have accepted the fact that vascular calcification is not a passive process but a highly complex, cell mediated, active process in patients with cardiovascular disease (CVD) resulting from, metabolic insults of bone fragility, diabetes, hypertension, dyslipidemia and atherosclerosis. Over the years, studies have revealed various mechanisms of vascular calcification like induction of bone formation, apoptosis, alteration in Ca-P balance and loss of inhibition. Novel clinical studies targeting cellular mechanisms of calcification provide promising and potential avenues for drug development. The interventions include phosphate binders, sodium thiosulphate, vitamin K, calcimimetics, vitamin D, bisphosphonates, Myoinositol hexaphosphate (IP6), Denosumab and TNAP inhibitors. Concurrently investigators are also working towards reversing or curing pathological calcification. This review focuses on the relationship of vascular calcification to clinical diseases, regulators and factors causing calcification including genetics which have been identified. At present, there is lack of any significant preventive measures for calcifications and hence this review explores further possibilities for drug development and treatment modalities.
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