The effects of iron overload on mitochondrial function, mitochondrial dynamics, and ferroptosis in cardiomyocytes

Area of Science:

• Cardiology
• Mitochondrial Biology
• Cell Death Mechanisms

Background:

• Iron overload cardiomyopathy (IOC) is a major cause of death in hemochromatosis.
• Mechanisms linking iron overload to cardiac dysfunction, mitochondrial issues, and impaired dynamics are poorly understood.
• Ferroptosis, a regulated cell death form, is implicated in IOC, but its direct link to cardiac iron overload needs clarification.

Purpose of the Study:

• To comprehensively review the effects of iron overload on cardiac function.
• To elucidate the role of iron in cardiomyocyte ferroptosis and mitochondrial dynamics.
• To consolidate current knowledge and identify research gaps in iron-induced cardiac dysfunction.

Main Methods:

• Systematic review of in vitro and in vivo studies.
• Analysis of literature on iron's impact on cardiac mitochondria, ferroptosis, and left ventricular function.
• Synthesis of consistent and controversial findings.

Main Results:

• Iron overload significantly impairs cardiac mitochondrial function and dynamics.
• Cardiac iron accumulation promotes ferroptosis in cardiomyocytes.
• These molecular changes contribute to the deterioration of left ventricular function.

Conclusions:

• Cardiac iron overload adversely affects mitochondrial health and promotes ferroptosis, leading to IOC.
• Further mechanistic studies are needed to fully understand iron-induced cardiac dysfunction for clinical applications.