Tetranectin and Paraoxonase-1 as Markers of Heart Failure.

Background and

Objectives

This narrative review evaluates the potential of Tetranectin (TN) and Paraoxonase-1 (PON1) to bridge the gap between biological pathology and clinical risk stratification by mapping the "Fibrosis-Oxidative Axis". Materials and

Methods

A targeted literature search was conducted using Scopus, PubMed, and Google Scholar to identify studies examining the diagnostic and prognostic value of TN and PON1 in heart failure (HF). Evidence was synthesized qualitatively to analyze their roles in structural fibrosis and oxidative defense.

Results

Tetranectin functions as a structural indicator, where its dynamics reflect fibroblast activation, extracellular matrix (ECM) deposition, and protein sequestration during tissue remodeling. On the other hand, PON1 serves as a functional metabolic barometer; its reduced activity correlates with systemic oxidative burden, loss of endothelial protection, and pro-inflammatory signaling. These markers capture a bidirectional pathology where oxidative injury drives fibrotic remodeling, which subsequently continue metabolic dysfunction. A dual-biomarker profile is proposed to stratify disease activity: early-stage metabolic stress (reduced PON1) precedes structural changes, while progressive HF involves active fibrosis (altered TN) alongside persistent oxidative injury.

Conclusions

The combined assessment of TN and PON1 offers a complementary approach to HF profiling, potentially refining risk stratification beyond hemodynamic parameters. However, clinical implementation requires large-scale validation to address standardization issues and specificity limitations regarding multimorbidity.