Research on Vascular Calcification in Cardiovascular Disease

Dear Colleagues,

The ageing population continues to suffer from its primary killer: cardiovascular disease (CVD). Despite recent advances in interventional medicinal and surgical therapies, coronary artery disease is still the single most common cause of death. Modern cardiology is focused on techniques designed to restore blood flow in obstructed arteries. However, this reactive strategy is unable to save the life of approximately ~1.3 million patients per year that succumb to the initial coronary event. And although pharmacotherapy with agents such as antithrombotics and statins has proven to lower the risk of future CV events, it does not represent a remedy for all.

Vascular calcification (VC) has proven to play an important role in cardiovascular morbidity and mortality (and stroke). Indeed, vascular calcification plays a role in 4 out of the top 10 causes of death as postulated by the WHO. Previously thought to be a passive process, it is now clear vascular calcification is a highly regulated process involving many different factors.

Vascular calcification might present in different ways: it can occur in the vascular intima as well as in the media and it may have different shapes and sizes. Additionally, it can present in the aortic valves where it is related to aortic valve stenosis. Recent data suggest that microcalcification can have a destabilising effect on atherosclerotic plaques, whereas the role of large calcification plaque-stability is largely unknown. Rupture of an unstable (vulnerable) plaque is widely recognised as the principal precipitant of AMI and stroke and an important cause of death. Calcification of the medial vessel wall is strongly associated with hypertension and aneurysm. Comorbidities such as diabetes mellitus and chronic kidney disease fuel the vascular calcification process and are associated with increased cardiovascular mortality. Here, calcifying protein particles (CPPs) seem to play a major role.

Effective interventions to prevent and/or reverse vulnerable plaque formation and/or its rupture are lacking. This is largely due to the absence of insights in calcification pathophysiology and the translation thereof into cost-effective interventions. This illustrates the high promise of VC as new target for diagnosis and intervention in cardiovascular diseases, and a comprehensive view on initiation and progression of calcification and its impact on cardiovascular disease remains elusive. More importantly even, there is an urgent need to translate experimental findings into adequate diagnostic, preventive and therapeutic solutions.

The present Special Issue aims to summarize some of the newest advances in vascular calcification in CVD. We aim to highlight the key involvement of resident and infiltrated cells in the pathophysiology of CVD, including reviews focused on specific cell types. Also, we aim for biological, chemical, and medical expertise supporting a translational approach that will enable development of new or the evaluation of existing imaging modalities for the identification of vascular calcification for better risk prediction and benefit to patients. Finally, we aim for novel insights in treatment of – including vascular senescence – that lie behind the processes of calcification and altering of functionality of vascular tissue.

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• cardiovascular system
• cardiovascular disease
• vascular calcification
• calcifying protein particles (CPP)
• chronic kidney disease
• diabetes mellitus
• matrix gla protein
• vitamin K
• hypertension
• atrial fibrillation
• monckebergssclerosis
• medial calcifciation
• atherosclerosis
• thrombosis
• coagulation
• (myo)fibroblasts
• pericytes
• endothelium
• vascular smooth muscle cells
• macrophages
• platelets
• imaging
• MSCT
• NaF18