Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases

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Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases. / Kjaergaard, A.D.; Johansen, Julia Sidenius; Bojesen, Stig Egil; Nordestgaard, Børge.

In: Critical Reviews in Clinical Laboratory Sciences, Vol. 53, No. 6, 2016, p. 396-408.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Kjaergaard, AD, Johansen, JS, Bojesen, SE & Nordestgaard, B 2016, 'Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases', Critical Reviews in Clinical Laboratory Sciences, vol. 53, no. 6, pp. 396-408. https://doi.org/10.1080/10408363.2016.1190683

APA

Kjaergaard, A. D., Johansen, J. S., Bojesen, S. E., & Nordestgaard, B. (2016). Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases. Critical Reviews in Clinical Laboratory Sciences, 53(6), 396-408. https://doi.org/10.1080/10408363.2016.1190683

Vancouver

Kjaergaard AD, Johansen JS, Bojesen SE, Nordestgaard B. Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases. Critical Reviews in Clinical Laboratory Sciences. 2016;53(6):396-408. https://doi.org/10.1080/10408363.2016.1190683

Author

Kjaergaard, A.D. ; Johansen, Julia Sidenius ; Bojesen, Stig Egil ; Nordestgaard, Børge. / Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases. In: Critical Reviews in Clinical Laboratory Sciences. 2016 ; Vol. 53, No. 6. pp. 396-408.

Bibtex

@article{72f51a788dc54459aed1c49b29df0702,
title = "Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases",
abstract = "This review summarizes present evidence for the role of YKL-40 in the diagnosis, prognosis and cause of cardiovascular and alcoholic liver disease. The question of whether YKL-40 is merely a marker or a causal factor in the development of cardiovascular and liver disease is addressed, with emphasis on the Mendelian randomization design. The Mendelian randomization approach uses genetic variants associated with lifelong high plasma YKL-40 levels that are largely unconfounded and not prone to reverse causation. Thus, the approach mimics a controlled double-blind randomized trial, but it uses genetic variants rather than a drug and placebo, and like a blinded trial, it allows inference about causality. Moreover, the review also covers background on the molecular biology and functions of YKL-40, YKL-40 levels in healthy individuals and reference range, and the role of YKL-40 as a biomarker of cardiovascular and alcoholic liver disease. YKL-40 is a plasma protein named after its three N-terminal amino acids, Y (tyrosine), K (lysine) and L (leucine), and its molecular weight of 40 kDa. It is produced by local inflammatory cells in inflamed tissues, such as lipid-laden macrophages inside the vessel wall and perhaps also hepatic stellate cells. Observational studies show that plasma YKL-40 levels are elevated in patients with cardiovascular and liver disease and are associated with disease severity and prognosis. Furthermore, elevated plasma YKL-40 levels in apparently healthy individuals are associated with a 2-fold increased risk of future ischemic stroke and venous thromboembolism, but not with myocardial infarction, suggesting that YKL-40 could play a role in the formation of embolisms rather than atherosclerosis per se. Further, elevated YKL-40 levels combined with excessive alcohol consumption are associated with 10-years risk of alcoholic liver cirrhosis of up to 7{\%}, suggesting that YKL-40 can be used as a strong noninvasive marker of predicting alcoholic liver cirrhosis. Importantly, in Mendelian randomization studies, genetically elevated plasma YKL-40 levels were not associated with risk of cardiovascular and alcoholic liver disease, thus suggesting that plasma YKL-40 does not play a causal role in the development of these diseases. Despite this, plasma YKL-40 levels may play a role in disease progression after diagnosis, and inhibition of YKL-40 activity might be a novel therapy in some cardiovascular and liver diseases.",
keywords = "Journal Article",
author = "A.D. Kjaergaard and Johansen, {Julia Sidenius} and Bojesen, {Stig Egil} and B{\o}rge Nordestgaard",
year = "2016",
doi = "10.1080/10408363.2016.1190683",
language = "English",
volume = "53",
pages = "396--408",
journal = "Critical Reviews in Clinical Laboratory Sciences",
issn = "1040-8363",
publisher = "Taylor & Francis",
number = "6",

}

RIS

TY - JOUR

T1 - Role of inflammatory marker YKL-40 in the diagnosis, prognosis and cause of cardiovascular and liver diseases

AU - Kjaergaard, A.D.

AU - Johansen, Julia Sidenius

AU - Bojesen, Stig Egil

AU - Nordestgaard, Børge

PY - 2016

Y1 - 2016

N2 - This review summarizes present evidence for the role of YKL-40 in the diagnosis, prognosis and cause of cardiovascular and alcoholic liver disease. The question of whether YKL-40 is merely a marker or a causal factor in the development of cardiovascular and liver disease is addressed, with emphasis on the Mendelian randomization design. The Mendelian randomization approach uses genetic variants associated with lifelong high plasma YKL-40 levels that are largely unconfounded and not prone to reverse causation. Thus, the approach mimics a controlled double-blind randomized trial, but it uses genetic variants rather than a drug and placebo, and like a blinded trial, it allows inference about causality. Moreover, the review also covers background on the molecular biology and functions of YKL-40, YKL-40 levels in healthy individuals and reference range, and the role of YKL-40 as a biomarker of cardiovascular and alcoholic liver disease. YKL-40 is a plasma protein named after its three N-terminal amino acids, Y (tyrosine), K (lysine) and L (leucine), and its molecular weight of 40 kDa. It is produced by local inflammatory cells in inflamed tissues, such as lipid-laden macrophages inside the vessel wall and perhaps also hepatic stellate cells. Observational studies show that plasma YKL-40 levels are elevated in patients with cardiovascular and liver disease and are associated with disease severity and prognosis. Furthermore, elevated plasma YKL-40 levels in apparently healthy individuals are associated with a 2-fold increased risk of future ischemic stroke and venous thromboembolism, but not with myocardial infarction, suggesting that YKL-40 could play a role in the formation of embolisms rather than atherosclerosis per se. Further, elevated YKL-40 levels combined with excessive alcohol consumption are associated with 10-years risk of alcoholic liver cirrhosis of up to 7%, suggesting that YKL-40 can be used as a strong noninvasive marker of predicting alcoholic liver cirrhosis. Importantly, in Mendelian randomization studies, genetically elevated plasma YKL-40 levels were not associated with risk of cardiovascular and alcoholic liver disease, thus suggesting that plasma YKL-40 does not play a causal role in the development of these diseases. Despite this, plasma YKL-40 levels may play a role in disease progression after diagnosis, and inhibition of YKL-40 activity might be a novel therapy in some cardiovascular and liver diseases.

AB - This review summarizes present evidence for the role of YKL-40 in the diagnosis, prognosis and cause of cardiovascular and alcoholic liver disease. The question of whether YKL-40 is merely a marker or a causal factor in the development of cardiovascular and liver disease is addressed, with emphasis on the Mendelian randomization design. The Mendelian randomization approach uses genetic variants associated with lifelong high plasma YKL-40 levels that are largely unconfounded and not prone to reverse causation. Thus, the approach mimics a controlled double-blind randomized trial, but it uses genetic variants rather than a drug and placebo, and like a blinded trial, it allows inference about causality. Moreover, the review also covers background on the molecular biology and functions of YKL-40, YKL-40 levels in healthy individuals and reference range, and the role of YKL-40 as a biomarker of cardiovascular and alcoholic liver disease. YKL-40 is a plasma protein named after its three N-terminal amino acids, Y (tyrosine), K (lysine) and L (leucine), and its molecular weight of 40 kDa. It is produced by local inflammatory cells in inflamed tissues, such as lipid-laden macrophages inside the vessel wall and perhaps also hepatic stellate cells. Observational studies show that plasma YKL-40 levels are elevated in patients with cardiovascular and liver disease and are associated with disease severity and prognosis. Furthermore, elevated plasma YKL-40 levels in apparently healthy individuals are associated with a 2-fold increased risk of future ischemic stroke and venous thromboembolism, but not with myocardial infarction, suggesting that YKL-40 could play a role in the formation of embolisms rather than atherosclerosis per se. Further, elevated YKL-40 levels combined with excessive alcohol consumption are associated with 10-years risk of alcoholic liver cirrhosis of up to 7%, suggesting that YKL-40 can be used as a strong noninvasive marker of predicting alcoholic liver cirrhosis. Importantly, in Mendelian randomization studies, genetically elevated plasma YKL-40 levels were not associated with risk of cardiovascular and alcoholic liver disease, thus suggesting that plasma YKL-40 does not play a causal role in the development of these diseases. Despite this, plasma YKL-40 levels may play a role in disease progression after diagnosis, and inhibition of YKL-40 activity might be a novel therapy in some cardiovascular and liver diseases.

KW - Journal Article

U2 - 10.1080/10408363.2016.1190683

DO - 10.1080/10408363.2016.1190683

M3 - Review

C2 - 27187575

VL - 53

SP - 396

EP - 408

JO - Critical Reviews in Clinical Laboratory Sciences

JF - Critical Reviews in Clinical Laboratory Sciences

SN - 1040-8363

IS - 6

ER -

ID: 174859867