Soluble CD146 in Heart Failure: Pathophysiological Role and Diagnostic Potential

TL;DR

This paper reviews the role of soluble CD146 as a potential biomarker for heart failure, highlighting its connection to vascular stress and diagnostic potential.

Contribution

The paper introduces sCD146 as a novel biomarker reflecting endothelial stress and hemodynamic congestion in heart failure.

Findings

Elevated sCD146 levels correlate with congestion indicators and adverse outcomes in heart failure.

sCD146 is released due to endothelial stress and inflammation, making it a potential diagnostic marker.

Its clinical use is limited by variability and non-cardiac confounders like malignancy.

Abstract

Heart failure (HF) remains a major global health challenge, driven by multifactorial pathophysiological processes, such as systemic congestion, endothelial dysfunction, and inflammation. While natriuretic peptides are well-established biomarkers for diagnosing and monitoring HF, they do not fully capture the complexity of vascular involvement. CD146, also known as melanoma cell adhesion molecule (MCAM), is a transmembrane glycoprotein primarily expressed on endothelial cells and involved in cell adhesion, vascular permeability, and angiogenesis. Its soluble form (sCD146), released in response to multiple pathophysiological stimuli, including venous and arterial endothelial stretch, oxidative stress, and inflammatory cytokine activation, has emerged as a promising biomarker reflecting both hemodynamic congestion and systemic endothelial stress. This review synthesizes current knowledge on the structure, regulation, and release mechanisms of CD146 and explores its clinical utility in HF. Elevated sCD146 levels have been associated with echocardiographic and radiological indicators of congestion, as well as with adverse outcomes. While promising, its application is limited by variability, lack of standardization, and confounding elevations in non-cardiac conditions, including malignancy.

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