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. 2017 Jun;13(4):897-913.
doi: 10.5114/aoms.2016.58664. Epub 2016 Mar 22.

Potential novel biomarkers of cardiovascular dysfunction and disease: cardiotrophin-1, adipokines and galectin-3

Affiliations

Potential novel biomarkers of cardiovascular dysfunction and disease: cardiotrophin-1, adipokines and galectin-3

Simona Hogas et al. Arch Med Sci. 2017 Jun.

Abstract

Cardiovascular disease is one of the main burdens of healthcare systems worldwide. Nevertheless, assessing cardiovascular risk in both apparently healthy individuals and low/high-risk patients remains a difficult issue. Already established biomarkers (e.g. brain natriuretic peptide, troponin) have significantly improved the assessment of major cardiovascular events and diseases but cannot be applied to all patients and in some cases do not provide sufficiently accurate information. In this context, new potential biomarkers that reflect various underlying pathophysiological cardiac and vascular modifications are needed. Also, a multiple biomarker evaluation that shows changes in the cardiovascular state is of interest. This review describes the role of selected markers of vascular inflammation, atherosclerosis, atherothrombosis, endothelial dysfunction and cardiovascular fibrosis in the pathogenesis and prognosis of cardiovascular disease: the potential use of cardiotrophin-1, leptin, adiponectin, resistin and galectin-3 as biomarkers for various cardiovascular conditions is discussed.

Keywords: adipokines; cardiotrophin-1; cardiovascular disease; galectin-3.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of CT-1 signaling pathways and their different effects on the cardiac cell (see text for abbreviations)
Figure 2
Figure 2
Schematic representation of actions of leptin ED – endothelial dysfunction, IL-6 – interleukin 6, IL-4 – interleukin 4, TNF-α – tumor necrosis factor α.
Figure 3
Figure 3
Schematic representation of adiponectin actions ED – endothelial dysfunction, TNF-α – tumor necrosis factor α, VSMCs – vascular smooth muscle cells, eNOS – endothelial nitric oxide synthase, NO – nitric oxide, ROS – reactive oxygen species.
Figure 4
Figure 4
Schematic representations of resistin actions ED – endothelial dysfunction, NO – nitric oxide, NF-κB – nuclear factor κB, ACE – angiotensin converting enzyme, TNFRSF1At – tumor necrosis factor receptor superfamily member 1A, TNF-α – tumor necrosis factor α, VSMCs – vascular smooth muscle cells.
Figure 5
Figure 5
Schematic representation of galectin-3 actions VSMCs – vascular smooth muscle cells.

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