New study on prioritizing targets in the circulating proteome for putative cardiac origin in heart failure. Co-led by Dr. Tucker and collaborators from Vanderbilt University Medical Center (Ravi Shah and Quinn Wells), Boston University (Matthew Nayor) and Northwestern University (Sadiya Khan)
Summary from https://doi.org/10.1016/j.xcrm.2024.101704
Given expanding studies in epidemiology and disease-oriented human studies offering hundreds of associations between the human “ome” and disease, prioritizing molecules relevant to disease mechanisms among this growing breadth is important. Here, we link the circulating proteome to human heart failure (HF) propensity (via echocardiographic phenotyping and clinical outcomes) across the lifespan, demonstrating key pathways of fibrosis, inflammation, metabolism, and hypertrophy. We observe a broad array of genes encoding proteins linked to HF phenotypes and outcomes in clinical populations dynamically expressed at a transcriptional level in human myocardium during HF and cardiac recovery (several in a cell-specific fashion). Many identified targets do not have wide precedent in large-scale genomic discovery or human studies, highlighting the complementary roles for proteomic and tissue transcriptomic discovery to focus epidemiological targets to those relevant in human myocardium for further interrogation.
Our role was the reanalysis of single nucleus sequencing data from published sources, with a goal of bringing some of the proteomic targets back to the tissue itself.
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