Mitochondria are the powerhouses of our cells, responsible for producing energy through oxidative metabolism. When these structures become damaged—such as during heart injury—the result can be severe oxidative stress and impaired energy production. Recent research examined how hyperbaric oxygen therapy (HBOT) affects mitochondrial function and autophagy in a model of myocardial ischemia-reperfusion injury (MIRI), a condition caused by temporary loss and restoration of blood flow to the heart.
Study Overview
Researchers used a rat model in which the left anterior descending (LAD) artery was ligated to mimic heart injury. HBOT was administered once daily for 14 days in a 0.25 MPa (approximately 2.5 ATA) chamber before the injury occurred. The goal was to determine whether HBOT could protect mitochondria and reduce cellular damage through improved oxygen utilization and metabolic regulation.
Measurements were conducted using ELISA, fluorescent probes, transmission electron microscopy, RT-qPCR, and immunohistochemistry to evaluate mitochondrial health, autophagy, and energy-related molecules.
Key Findings
- Enhanced Energy Production: HBOT pretreatment increased levels of ATP, ADP, and overall energy charge, while reducing AMP, signaling improved mitochondrial output.
- Improved Mitochondrial Morphology: Electron microscopy showed healthier mitochondrial structures and fewer autophagic vesicles in HBOT-treated hearts.
- Reduced Oxidative Stress: Reactive oxygen species (ROS) and cytochrome c release decreased following treatment, indicating less oxidative injury and apoptosis.
- Gene Expression Shifts: HBOT boosted beneficial mitochondrial and metabolic genes—such as mTOR, mitofusin 1 and 2, and NADH dehydrogenase subunit 1—while downregulating autophagy-related genes like Atg5 and p53.
Scientific Perspective
These findings indicate that hyperbaric oxygen therapy restores mitochondrial function by balancing oxygen supply and metabolic demand, supporting energy production, and reducing autophagy-driven cell loss. By protecting mitochondria from dysfunction, HBOT may help preserve cardiac tissue during and after ischemic events.
Research Implications
While this study focused on animal models, it adds to growing evidence that HBOT’s cellular benefits extend beyond wound healing—potentially influencing mitochondrial health across organ systems. Future research will be needed to explore how these mechanisms translate to clinical use in humans with cardiovascular or metabolic disorders.
Check out the PubMed article here: https://pubmed.ncbi.nlm.nih.gov/32901878/
