Article Abstract

Role of “osteogenic” cardiac fibroblasts in pathological heart calcification

Authors: Hong Zhan, Toru Suzuki

Abstract

Calcification of mammalian soft tissues as induced by age and injury is a cell mediated process that resembles bone formation in the skeletal system with calcification of the extracellular matrix by cells capable of mineralization (1). The abnormal accumulation of calcium salts occurs in the pathologic calcification of any tissue (2). Two basic forms of calcification are recognized; dystrophic and metastatic (3). Ischemic, traumatic, infectious and/or inflammatory, and neoplastic processes among others are significant causes of dystrophic myocardial calcification. Any abnormality of calcium metabolism can lead to metastatic myocardial calcification, including chronic renal failure, bone destruction or increased bone turnover, hyperparathyroidism, and vitamin D-related disorders. Calcification of the cardiovascular system, such as aortic valve and vascular calcification, has important clinical significance (4). Myocardial calcification is an unusual form of soft tissue calcification characterized by abnormal calcific accumulation within the heart muscle which can occur in the absence of calcification of vessels, valves, or other organs (5). Calcification within the myocardium is one of the most common underlying causes of heart block where calcification and fibrosis of the conduction system interrupts smooth propagation of electrical impulses (6). The occurrence of heart muscle calcification is observed in senile heart diseases and in varieties of disease conditions, such as chronic renal disease, diabetes, and myocardial injury secondary to inflammation or ischemia (7). However, the identity of cells and the mechanism contributing to pathological myocardial calcification has remained elusive.

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