Guanidinylated ApoA-I accumulation in CKD progression: impaired anti-inflammatory properties

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Guanidinylated ApoA-I accumulation in CKD progression: impaired anti-inflammatory properties

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Co-author 1

Joachim Jankowski jjankowski@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany *

Co-author 2

Emiel van der Vorst vandervorst@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany -

Co-author 3

Vera Jankowski vjankowski@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany -

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Introduction

Chronic kidney disease (CKD) substantially heightens the likelihood of cardiovascular events, in part due to the impaired functionality of high-density lipoprotein (HDL) and its connection with atherosclerosis.

Methods

In this study, 84 patients with CKD stages 2-5 were included, and plasma was isolated and analysed using mass spectrometry to detect post-translational modifications of apolipoprotein A-I (apoA-I), the main protein component of HDL.

Results

Guanidinylation, a non-enzymatic post-translational modification, increased levels of apoA-I with CKD progression; significant modifications were observed in apoA-I in patients with CKD stage 3 onwards. The observed modification patterns of apoA-I in CKD patients were mimicked in vitro. This modified apoA-I was used for functional assays, which revealed that guanidinylation compromised the anti-inflammatory and anti-oxidative properties of apoA-I, which supports the relevance of the clinical findings. Specifically, guanidinylated apoA-I activated inflammatory kinases in macrophages, suggesting a mechanistic link between apoA-I modifications and inflammatory responses. These findings suggest potential alterations in the functional properties of apoA-I in CKD patients due to guanidinylation.

Conclusion

The identification of guanidinylated apoA-I peptides in plasma highlights a novel aspect of protein modification in CKD pathophysiology. Therefore, the results of this study may contribute to a better understanding of the molecular mechanisms underlying CKD-related cardiovascular complications and highlight the importance and the need to prevent post-translational modifications in CKD patients

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