Identification and validation of STEAP3 as a ferroptosis-related biomarker in heart failure

By
Huijuan Chen
Lingqi Xu
June 1, 2026
0 min

Frontiers In Cardiovascular Medicine

Overview

This study identifies STEAP3 as a potential biomarker linked to ferroptosis in heart failure (HF). The findings suggest that aging-related programmed cell death (PCD) genes play a significant role in HF pathology, highlighting the need for further clinical validation.

Background

Heart failure is a prevalent clinical syndrome with a poor prognosis, often exacerbated by aging and programmed cell death mechanisms. Understanding the molecular underpinnings of HF, particularly the role of aging-related PCD, is crucial for developing effective diagnostic and therapeutic strategies. This study aims to elucidate the relationship between these factors and identify potential biomarkers for improved patient outcomes.

Data Highlights

No numerical data available in the source material.

Key Findings

Ferroptosis, autophagy, and necroptosis are correlated with aging in heart failure.
Eighteen differentially expressed aging-related PCD genes were identified.
The LASSO model demonstrated superior diagnostic performance for HF.
Significant differences in immune microenvironment were noted between aging-PCD index-high and index-low groups.
STEAP3 may contribute to ferroptosis-related injury in cardiomyocytes via glutathione metabolism and iron homeostasis.

Clinical Implications

The identification of STEAP3 as a biomarker associated with ferroptosis in HF may guide future diagnostic and therapeutic approaches. Understanding the interplay between aging, PCD, and HF could lead to personalized treatment strategies that improve patient outcomes.

Conclusion

The study underscores the importance of aging-related PCD in heart failure and presents STEAP3 as a promising biomarker for further investigation. These findings could pave the way for novel therapeutic interventions targeting ferroptosis.