Proteomic signature of HIV-associated subclinical left atrial remodeling and incident heart failure.

Tess E Peterson, Virginia S Hahn, Ruin Moaddel, Min Zhu, Sabina A Haberlen, Frank J Palella, Michael Plankey, Joel S Bader, Joao A C Lima, Robert E Gerszten, Jerome I Rotter, Stephen S Rich, Susan R Heckbert, Gregory D Kirk, Damani A Piggott, Luigi Ferrucci, Joseph B Margolick, Todd T Brown, Katherine C Wu, Wendy S Post

Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA. [email protected] of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA. [email protected]. · pubmed

Paper

Abstract

People living with HIV are at higher risk of heart failure and associated left atrial remodeling compared to people without HIV. Mechanisms are unclear but have been linked to inflammation and premature aging. Here we obtain plasma proteomics concurrently with cardiac magnetic resonance imaging in two independent study populations to identify parallels between HIV-related and aging-related immune dysfunction that could contribute to atrial remodeling and clinical heart failure. We discover a plasma proteomic signature that may in part reflect or contribute to HIV-associated atrial remodeling, many features of which are associated with older age and time to incident heart failure among an independent community-based cohort without HIV. This proteomic profile was statistically enriched for immune checkpoint proteins, tumor necrosis factor signaling, ephrin signaling, and extracellular matrix organization, identifying possible shared pathways in HIV and aging that may contribute to risk of heart failure.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper explores the proteomic signature associated with HIV-related heart failure and its parallels with aging-related immune dysfunction, which touches on mechanisms that could be linked to aging processes. However, while it identifies potential shared pathways, it primarily focuses on a specific disease context rather than addressing the root causes of aging or lifespan extension. Thus, it presents solid research but with limited broader implications for the field of longevity.

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