Mitochondrial Dysfunction and Therapeutic Perspectives in Cardiovascular Diseases

Area of Science:

• Biochemistry
• Cardiology
• Mitochondrial Biology

Background:

• Cardiovascular diseases (CVDs) exhibit high mortality rates globally.
• Mitochondrial dysfunction, particularly involving mitochondrial DNA (mtDNA) mutations, is a key factor in CVD pathogenesis.
• mtDNA mutations disrupt oxidative phosphorylation (OXPHOS), ATP production, and increase reactive oxygen species (ROS).

Purpose of the Study:

• To analyze the link between mtDNA mutations, mitophagy, OXPHOS, ROS, and CVDs from a mitochondrial dysfunction perspective.
• To explore and evaluate current therapeutic strategies for CVDs targeting mitochondrial dysfunction.

Main Methods:

• Literature review and analysis of the relationship between mitochondrial factors and CVDs.
• Discussion of therapeutic strategies including mtDNA editing, mitochondrial replacement, mitophagy enhancement, OXPHOS improvement, and ROS reduction.

Main Results:

• Mitochondrial dysfunction, characterized by mtDNA mutations, impaired mitophagy, reduced OXPHOS, and elevated ROS, is strongly associated with CVDs.
• Various therapeutic strategies show potential but face limitations in safety and clinical efficacy.

Conclusions:

• Addressing mitochondrial dysfunction presents a promising frontier for CVD treatment development.
• Despite challenges, targeting mtDNA mutations and related mitochondrial pathways offers hope for future cardiovascular therapies.