Mitochondrial Integrity Is Critical in Right Heart Failure Development.

Area of Science:

• Cardiology
• Mitochondrial Biology
• Heart Failure Pathophysiology

Background:

• Right ventricular dysfunction (RVD) and right heart failure (RHF) affect a growing patient population with limited therapeutic options.
• Mitochondrial dysfunction, including impaired energy production and increased oxidative stress, is increasingly recognized as a critical cellular mechanism in RHF.
• Existing treatments for RHF are insufficient, highlighting the need for a deeper understanding of underlying molecular pathways.

Purpose of the Study:

• To comprehensively review current knowledge on mitochondrial dysregulation in preclinical and clinical RVD and RHF.
• To analyze the relationship between mitochondrial processes and the functional capacity of the right ventricle (RV).
• To identify potential therapeutic targets by elucidating the role of mitochondria in RHF pathogenesis.

Main Methods:

• Systematic literature review of preclinical and clinical studies on mitochondrial function in RVD and RHF.
• Analysis of molecular mechanisms including mitochondrial biogenesis, substrate metabolism, redox balance, and oxidative phosphorylation.
• Correlation of identified mitochondrial alterations with functional parameters of the right ventricle.

Main Results:

• Mitochondrial dysfunction significantly contributes to cardiomyocyte damage and impaired RV function in RHF.
• Alterations in mitochondrial biogenesis, substrate utilization, and oxidative phosphorylation are consistently observed in RVD and RHF.
• Increased reactive oxygen species production by mitochondria exacerbates RHF pathology.

Conclusions:

• Mitochondrial dysregulation is a central pathomechanistic process in the development and progression of RHF.
• Targeting mitochondrial pathways presents a promising therapeutic strategy for RHF.
• Further research is needed to translate findings on mitochondrial mechanisms into effective clinical interventions for RHF.