Profiling of the plasma proteome across different stages of human heart failure

Anna Egerstedt, John Berntsson, Maya Landenhed Smith, Olof Gidlöf, Roland Nilsson, Mark Benson, Quinn S. Wells, Selvi Celik, Carl Lejonberg, Laurie Farrell, Sumita Sinha, Dongxiao Shen, Jakob Lundgren, Göran Rådegran, Debby Ngo, Gunnar Engström, Qiong Yang, Thomas J. Wang, Robert E. Gerszten and J. Gustav Smith ()
Additional contact information
Anna Egerstedt: Lund University
John Berntsson: Lund University
Maya Landenhed Smith: Lund University and Skåne University Hospital
Olof Gidlöf: Lund University
Roland Nilsson: Karolinska Institutet and Karolinska University Hospital
Mark Benson: Beth Israel Deaconess Medical Center and Harvard Medical School
Quinn S. Wells: Vanderbilt University
Selvi Celik: Lund University
Carl Lejonberg: Lund University
Laurie Farrell: Beth Israel Deaconess Medical Center and Harvard Medical School
Sumita Sinha: Beth Israel Deaconess Medical Center and Harvard Medical School
Dongxiao Shen: Beth Israel Deaconess Medical Center and Harvard Medical School
Jakob Lundgren: Lund University
Göran Rådegran: Lund University
Debby Ngo: Beth Israel Deaconess Medical Center and Harvard Medical School
Gunnar Engström: Lund University
Qiong Yang: Boston University School of Public Health
Thomas J. Wang: Vanderbilt University
Robert E. Gerszten: Beth Israel Deaconess Medical Center and Harvard Medical School
J. Gustav Smith: Lund University

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Heart failure (HF) is a major public health problem characterized by inability of the heart to maintain sufficient output of blood. The systematic characterization of circulating proteins across different stages of HF may provide pathophysiological insights and identify therapeutic targets. Here we report application of aptamer-based proteomics to identify proteins associated with prospective HF incidence in a population-based cohort, implicating modulation of immunological, complement, coagulation, natriuretic and matrix remodeling pathways up to two decades prior to overt disease onset. We observe further divergence of these proteins from the general population in advanced HF, and regression after heart transplantation. By leveraging coronary sinus samples and transcriptomic tools, we describe likely cardiac and specific cellular origins for several of the proteins, including Nt-proBNP, thrombospondin-2, interleukin-18 receptor, gelsolin, and activated C5. Our findings provide a broad perspective on both cardiac and systemic factors associated with HF development.

Date: 2019
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DOI: 10.1038/s41467-019-13306-y

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