About this Research Topic
Extracellular matrix mineralization is a physiological process that provides our bones and teeth with their unique physical and mechanical properties. However, when this essential process occurs in the 'soft' tissues, it can be detrimental to health. 'Soft' tissue mineralization, often termed as ‘calcification’, is essentially a pathological event, which can affect a myriad of tissues including vascular tissues, skin, kidney, muscle and ‘soft’ cartilaginous tissues of the body. Several chronic disorders such as diabetes, atherosclerosis, chronic kidney diseases and osteoarthritis have been associated with ‘soft’ tissue calcification. 'Soft' tissue calcification can also be seen in several rare diseases, e.g. Keutel Syndrome, generalized arterial calcification in infancy, pseudoxanthoma elasticum and some forms of vitamin K-dependent clotting factor deficiency.
At present, the existing body of literature suggests that the mechanisms of ectopic mineralization in the ‘soft’ tissues can vary widely and may well depend on the etiology and the type of tissue where it occurs. The mechanism of ‘soft’ tissue calcification can be analogous to ectopic bone formation as seen in rare diseases like fibrodysplasia ossificans progressiva or more commonly as heterotopic ossification in shattered limbs and in the arteries of atherosclerotic patients. On the other hand, emerging data suggest that not all ‘soft’ tissue calcifications recapitulate the process of bone mineralization. For example, the loss of mineralization inhibitors can result in ‘soft’ tissue calcification without involving any induction of bone mineralization-related genes. In some cases, it was shown that the initial phases of ‘soft’ tissue calcification did not involve bone/cartilage markers, while at the later stages some of these markers were upregulated in the mineralizing tissues.
Although tremendous progress have been made over the last two decades, an incomplete understanding of the mechanism of normal and ectopic mineralization is seriously hampering the progress of developing novel therapeutic approaches to treat and/or manage the diseases associated with ectopic calcification.
This Research Topic on pathologic calcification intends to publish research and review articles covering the mechanisms of calcification of various biological tissues.
We welcome submissions covering the following topics:
• Studies on the development of new in vitro and in vivo models
• Clinical studies reporting novel forms of ectopic calcification
• Single-cell analysis on ectopic mineralization
• Signalling dysregulation in the microenvironment of ectopic Mineralization
• Small-molecule compounds targeting ectopic mineralization
• Biologics targeting ectopic mineralization.
Depending on the relevance, studies describing novel mechanisms of hard tissue mineralization will also be considered. The articles can be full-length or in the form of short reports. Please see the various Article Types accepted by Frontiers in Cell and Developmental Biology here.
At present, the existing body of literature suggests that the mechanisms of ectopic mineralization in the ‘soft’ tissues can vary widely and may well depend on the etiology and the type of tissue where it occurs. The mechanism of ‘soft’ tissue calcification can be analogous to ectopic bone formation as seen in rare diseases like fibrodysplasia ossificans progressiva or more commonly as heterotopic ossification in shattered limbs and in the arteries of atherosclerotic patients. On the other hand, emerging data suggest that not all ‘soft’ tissue calcifications recapitulate the process of bone mineralization. For example, the loss of mineralization inhibitors can result in ‘soft’ tissue calcification without involving any induction of bone mineralization-related genes. In some cases, it was shown that the initial phases of ‘soft’ tissue calcification did not involve bone/cartilage markers, while at the later stages some of these markers were upregulated in the mineralizing tissues.
Although tremendous progress have been made over the last two decades, an incomplete understanding of the mechanism of normal and ectopic mineralization is seriously hampering the progress of developing novel therapeutic approaches to treat and/or manage the diseases associated with ectopic calcification.
This Research Topic on pathologic calcification intends to publish research and review articles covering the mechanisms of calcification of various biological tissues.
We welcome submissions covering the following topics:
• Studies on the development of new in vitro and in vivo models
• Clinical studies reporting novel forms of ectopic calcification
• Single-cell analysis on ectopic mineralization
• Signalling dysregulation in the microenvironment of ectopic Mineralization
• Small-molecule compounds targeting ectopic mineralization
• Biologics targeting ectopic mineralization.
Depending on the relevance, studies describing novel mechanisms of hard tissue mineralization will also be considered. The articles can be full-length or in the form of short reports. Please see the various Article Types accepted by Frontiers in Cell and Developmental Biology here.
Keywords: Ectopic Calcification, Mineralization Inhibitors, Biomineralization, Mineral Homeostasis, Genetic Regulators of Biomineralization
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
