Calcium phosphate bions: towards a pathogenetic concept
Supersaturation of blood with calcium and phosphate is associated with higher risk of major adverse cardiovascular events; however, pathophysiological basis of such association remains unclear. Upon an excess of serum calcium and phosphate, mineral chaperone fetuin-A aggregates mineral ions into cal...
Saved in:
| Main Author: | |
|---|---|
| Format: | Article |
| Language: | Russian |
| Published: |
Kemerovo State Medical University
2020-03-01
|
| Series: | Фундаментальная и клиническая медицина |
| Subjects: | |
| Online Access: | https://fcm.kemsmu.ru/jour/article/view/224 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1839591860085981184 |
|---|---|
| author | A. G. Kutikhin |
| author_facet | A. G. Kutikhin |
| author_sort | A. G. Kutikhin |
| collection | DOAJ |
| description | Supersaturation of blood with calcium and phosphate is associated with higher risk of major adverse cardiovascular events; however, pathophysiological basis of such association remains unclear. Upon an excess of serum calcium and phosphate, mineral chaperone fetuin-A aggregates mineral ions into calcium phosphate bions (CPB, alternatively termed calciprotein particles), which are irreversibly internalised by endothelial cells causing lysosome membrane permeabilisation, non-specific inflammatory response and cell death. Altogether, these processes contribute to pathological microenvironment potentiating endothelial dysfunction, osteochondrogenic differentiation of vascular smooth muscle cells, and adventitial inflammation which in turn culminate into intimal hyperplasia and medial arterial calcification. Albeit the correlation between increased CPB count in the blood and higher risk of cardiovascular events/cardiovascular death has initially been found in patients with chronic kidney disease, recent investigations suggest similar scenario in patients with arterial hypertension and coronary artery disease without renal dysfunction testifying to the general pathophysiological mechanism. Here we discuss the existing data on how CPB do form and how they affect the development of cardiovascular disease. We further consider advantages and shortcomings of the relevant experimental models as well as diagnostic significance of measuring CPB in the serum and clinical potential of anti-CPP therapies for the patients with chronic kidney disease, coronary artery disease, and cerebrovascular disease. |
| format | Article |
| id | doaj-art-cf1caee9f8f641d2bc549895ccb6c36d |
| institution | Matheson Library |
| issn | 2500-0764 2542-0941 |
| language | Russian |
| publishDate | 2020-03-01 |
| publisher | Kemerovo State Medical University |
| record_format | Article |
| series | Фундаментальная и клиническая медицина |
| spelling | doaj-art-cf1caee9f8f641d2bc549895ccb6c36d2025-08-03T12:59:24ZrusKemerovo State Medical UniversityФундаментальная и клиническая медицина2500-07642542-09412020-03-0151789310.23946/2500-0764-2020-5-1-78-93193Calcium phosphate bions: towards a pathogenetic conceptA. G. Kutikhin0Research Institute for Complex Issues of Cardiovascular DiseasesSupersaturation of blood with calcium and phosphate is associated with higher risk of major adverse cardiovascular events; however, pathophysiological basis of such association remains unclear. Upon an excess of serum calcium and phosphate, mineral chaperone fetuin-A aggregates mineral ions into calcium phosphate bions (CPB, alternatively termed calciprotein particles), which are irreversibly internalised by endothelial cells causing lysosome membrane permeabilisation, non-specific inflammatory response and cell death. Altogether, these processes contribute to pathological microenvironment potentiating endothelial dysfunction, osteochondrogenic differentiation of vascular smooth muscle cells, and adventitial inflammation which in turn culminate into intimal hyperplasia and medial arterial calcification. Albeit the correlation between increased CPB count in the blood and higher risk of cardiovascular events/cardiovascular death has initially been found in patients with chronic kidney disease, recent investigations suggest similar scenario in patients with arterial hypertension and coronary artery disease without renal dysfunction testifying to the general pathophysiological mechanism. Here we discuss the existing data on how CPB do form and how they affect the development of cardiovascular disease. We further consider advantages and shortcomings of the relevant experimental models as well as diagnostic significance of measuring CPB in the serum and clinical potential of anti-CPP therapies for the patients with chronic kidney disease, coronary artery disease, and cerebrovascular disease.https://fcm.kemsmu.ru/jour/article/view/224calcium phosphate bionsmineral homeostasischronic kidney diseasecardiovascular eventsendothelial dysfunctionvascular calcificationatherosclerosis |
| spellingShingle | A. G. Kutikhin Calcium phosphate bions: towards a pathogenetic concept Фундаментальная и клиническая медицина calcium phosphate bions mineral homeostasis chronic kidney disease cardiovascular events endothelial dysfunction vascular calcification atherosclerosis |
| title | Calcium phosphate bions: towards a pathogenetic concept |
| title_full | Calcium phosphate bions: towards a pathogenetic concept |
| title_fullStr | Calcium phosphate bions: towards a pathogenetic concept |
| title_full_unstemmed | Calcium phosphate bions: towards a pathogenetic concept |
| title_short | Calcium phosphate bions: towards a pathogenetic concept |
| title_sort | calcium phosphate bions towards a pathogenetic concept |
| topic | calcium phosphate bions mineral homeostasis chronic kidney disease cardiovascular events endothelial dysfunction vascular calcification atherosclerosis |
| url | https://fcm.kemsmu.ru/jour/article/view/224 |
| work_keys_str_mv | AT agkutikhin calciumphosphatebionstowardsapathogeneticconcept |