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The circulating proteomic signature of alcohol-associated liver disease
Jay Luther, … , Esperance A. Schaefer, Russell P. Goodman
Jay Luther, … , Esperance A. Schaefer, Russell P. Goodman
Published July 22, 2022
Citation Information: JCI Insight. 2022;7(14):e159775. https://doi.org/10.1172/jci.insight.159775.
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Resource and Technical Advance Hepatology

The circulating proteomic signature of alcohol-associated liver disease

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Abstract

Despite being a leading cause of advanced liver disease, alcohol-associated liver disease (ALD) has no effective medical therapies. The circulating proteome, which comprises proteins secreted by different cells and tissues in the context of normal physiological function or in the setting of disease and illness, represents an attractive target for uncovering novel biology related to the pathogenesis of ALD. In this work, we used the aptamer-based SomaScan proteomics platform to quantify the relative concentration of over 1300 proteins in a well-characterized cohort of patients with the spectrum of ALD. We found a distinct circulating proteomic signature that correlated with ALD severity, including over 600 proteins that differed significantly between ALD stages, many of which have not previously been associated with ALD to our knowledge. Notably, certain proteins that were markedly dysregulated in patients with alcohol-associated hepatitis were also altered, to a lesser degree, in patients with subclinical ALD and may represent early biomarkers for disease progression. Taken together, our work highlights the vast and distinct changes in the circulating proteome across the wide spectrum of ALD, identifies potentially novel biomarkers and therapeutic targets, and provides a proteomic resource atlas for ALD researchers and clinicians.

Authors

Jay Luther, Augustin G.L. Vannier, Esperance A. Schaefer, Russell P. Goodman

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Figure 1

The proteomic signature of ALD.

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The proteomic signature of ALD.
(A) Relative log2 fold abundance of each...
(A) Relative log2 fold abundance of each of 1305 proteins for each patient (n = 93) by clinical diagnosis. (B) Cluster dendrogram of patients versus relative protein abundance with clinical diagnosis and clinical characteristics. (C) PCA of relative protein abundance grouped by clinical diagnosis.

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