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Cell free DNA as a diagnostic and prognostic marker for cardiovascular diseases

*Corresponding author for this work
Scholary Output:
Contribution to journal
Review article
 Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Release of cell free DNA (cfDNA) from damaged or dead cells routinely occurs in normal physiology. Recently, cfDNA has emerged as an essential biomarker in cardiovascular disease (CVD) of potential prognostic and diagnostic significance. Within the last decade, significant research efforts have been devoted to uncovering the mechanisms mediating cfDNA release and its outcome-predicting ability. The current review focuses on the pathways for cfDNA release in myocardial infarction, heart failure and hypertension, and discusses implementation of cfDNA monitoring to assess the overall development of these disease states and predict future complications.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
 Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 145-150 (6 pages)

Journal (Volume, Issue Number)

Clinica Chimica Acta (Volume 503)

Publication milestones

  • Published - 04/2020

Publication status

Published - 04/2020

ISSN

0009-8981

Publication IDs

  • Scopus: 85078128992
  • PubMed: 31978408

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Scopus
citations
67, opens in new tab
Fractional count
1
Fractional count
0.33
Fractional count
2
Fractional count
0.67
Fractional count
1
Fractional count
1

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Citation count
67
Captures
70

Funding Details

This work was supported by the National Institute of Health (NIDDK) R00DK105160 to DVI, (NIDA) U54DA016511 to KYD-P and DVI, and the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award IK2BX003922 to KYD-P. This work was also financially supported, in part, by the 2019 S&R Foundation Ryuji Ueno Award that was bestowed upon KYD-P by the American Physiological Society. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the Veterans Administration, or the American Physiological Society. This work was supported by the National Institute of Health (NIDDK) R00DK105160 to DVI, (NIDA) U54DA016511 to KYD-P and DVI, and the Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award IK2BX003922 to KYD-P. This work was also financially supported, in part, by the 2019 S&R Foundation Ryuji Ueno Award that was bestowed upon KYD-P by the American Physiological Society. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the Veterans Administration, or the American Physiological Society.
FundersFunding numbers
S. S. DeYoung Foundation
-
NIH
IK2BX003922
NIDA
U54DA016511
NIDDK
R00DK105160
VA
-
APS
-
BLR&D, ORD
-