Redox Imbalance and Genetic Mutations in Heart Failure: Synergistic Mechanisms and Therapeutic Strategies

TL;DR

This review explores how redox imbalance and genetic mutations work together to cause heart failure and discusses potential treatments.

Contribution

The paper provides a comprehensive synthesis of the synergistic roles of redox signaling and genetic mutations in heart failure.

Findings

Redox imbalance and genetic mutations interact to drive cardiac dysfunction.

Current therapies targeting redox balance and genetic mutations show promise but have limitations.

Understanding the redox–genetic axis is crucial for developing new heart failure treatments.

Abstract

Heart failure (HF) is a significant global health challenge, with rising prevalence and a complex, multifactorial pathophysiology. Emerging evidence suggests that disruptions in redox signaling pathways and genetic mutations play critical, synergistic roles in the development and progression of HF. This comprehensive review synthesizes current knowledge on how redox imbalance and genetic alterations interact to drive cardiac dysfunction and critically evaluates the therapeutic strategies targeting these mechanisms. We begin by introducing the basic concepts of redox biology and its role in maintaining cardiac homeostasis. Next, we examine the specific redox signaling pathways and genetic mutations implicated in HF pathogenesis, highlighting the latest mechanistic insights and findings from human studies. The complex interplay between redox dysregulation and genetic factors is explored, including their synergistic effects, compensatory mechanisms, and illustrative case studies. We also review current therapeutic strategies aimed at restoring redox balance and correcting underlying genetic mutations, discussing their progress and limitations. Finally, we present the latest research advances, identify critical knowledge gaps, and propose future directions for both basic and translational research. Understanding the redox–genetic axis is key to developing novel, targeted therapies to address the growing HF epidemic.

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