4.7 Review

Soluble urokinase plasminogen activator receptor-A valuable biomarker in systemic lupus erythematosus?

Journal

CLINICA CHIMICA ACTA
Volume 444, Issue -, Pages 234-241

Publisher

ELSEVIER
DOI: 10.1016/j.cca.2015.02.031

Keywords

Soluble urokinase plasminogen activator receptor (suPAR); Systemic lupus erythematosus; Organ damage; Biomarker; Rheumatic disease; Nephritis

Funding

  1. Swedish Society for Medicine [SLS-253651, SLS-412701]
  2. Swedish Society against Rheumatism [R-385481, R-475441]
  3. Swedish Society for Medical Research
  4. Linkoping University Hospital Research Funds [LIO-378771, LIO-478621]
  5. King Gustaf V 80-year Foundation [FAI2014-0040]
  6. Professor Nanna Svartz Foundation

Ask authors/readers for more resources

Systemic lupus etythematosus (SLE) is a potentially severe autoimmune condition with an unpredictable-disease course, often with fluctuations in disease activity over time. Long term inflammation and drug-related side-effects may subsequently lead to permanent organ damage, a consequence which is intimately connected to decreased quality of life and mortality. New lupus biomarkers that convey information regarding inflammation and/or organ damage are thus warranted. Today, there is no clinical biomarker that indicates the risk of damage accrual. Herein we highlight the urokinase plasminogen activator receptor (uPAR) and especially its soluble form (suPAR) that besides having biological functions in e.g. proteolysis, cell migration and tissue homeostasis, recently has emerged as a promising biomarker of inflammation and prognosis of several disorders. A strong association between suPAR and organ damage in SLE was recently demonstrated, and preliminary data (presented in this review) suggests the possibility of a predictive value of suPAR blood levels. The involvement of suPAR in the pathogenesis of SLE remains obscure, but its effects in leukocyte recruitment, phagocytic uptake of dying cells (efferocytosis) and complement regulation suggests that the central parts of the SLE pathogenesis could be regulated by suPAR, and vice versa. (C) 2015 Elsevier B.V. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available