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Maria Gomez

Maria Gomez

Professor

Maria Gomez

Kv1.3 Channel, a Targetable Piece in the Complex Jigsaw Puzzle of Vascular Calcification?

Author

  • Maria F Gomez

Summary, in English

In parallel with an unprecedented progress in vascular and stem cell biology during the past two decades, our understanding of vascular calcification has evolved from being perceived as a harmless, passive deposition of minerals to what we now consider a highly regulated, cell-mediated process that is strongly associated with chronic kidney disease (CKD) and confers increased risk for incident cardiovascular disease. A PubMed search of the term “vascular calcification” reveals an impressive exponential growth in the number of original articles published between 2000-2015, but this trend seems to have slowed down in the past 5-6 years. Studies have helped us understand that vascular calcification can engage a large number of key mediators and signalling pathways and that its anatomical and histological location can determine the type and severity of the clinical outcomes. Despite this significantly increased knowledge regarding the underlying pathophysiology, very little progress has been made when it comes to therapies and only a handful of interventional studies have documented any impact on vascular calcification other than modest effects in slowing down the process. The reasons for this lack of translational progress are many, including a somewhat conventional view of vascular calcification with most interventions aiming at restoring or reverting the uremic environment or targeting calcification too late in the process.
In this issue of Function, Cazaña-Pérez et al provide new mechanistic insight in the regulation of vascular calcification, directing our attention to the vascular smooth muscle cell (VSMC), one of the main drivers in both medial and intimal calcification.

Department/s

  • Diabetic Complications
  • EXODIAB: Excellence in Diabetes Research in Sweden

Publishing year

2020-12-28

Language

English

Pages

1-3

Publication/Series

Function

Volume

2

Issue

1

Document type

Journal article (comment)

Publisher

Oxford University Press

Topic

  • Cardiac and Cardiovascular Systems

Status

Published

Research group

  • Diabetic Complications

ISBN/ISSN/Other

  • ISSN: 2633-8823