Oxidative Stress and Damaged Mitochondria Identified as Major Triggers of Heart Disease
Nikhil Prasad Fact checked by:Thailand Medical News Team Apr 13, 2025 10 months, 6 days, 11 hours, 23 minutes ago
Medical News: In a groundbreaking study, scientists have revealed how oxidative stress and mitochondrial dysfunction play a central role in the development and progression of various heart diseases, including heart failure, diabetic cardiomyopathy, and injury caused by restricted blood flow. The research—conducted by Dr. Naranjan S. Dhalla from the St. Boniface Hospital Albrechtsen Research Centre and the University of Manitoba in Canada, Dr. Petr Ostadal from Charles University and Motol University Hospital in the Czech Republic, and Dr. Paramjit S. Tappia from the Asper Clinical Research Institute in Canada—uncovered how damaged mitochondria, excessive reactive oxygen species (ROS), and disrupted calcium signaling contribute to heart dysfunction.
Oxidative Stress and Damaged Mitochondria Identified as Major Triggers of Heart Disease
This
Medical News report explores the study's detailed insights on how cellular stress causes mitochondrial malfunction, leading to cardiac muscle deterioration and energy failure in the heart. Mitochondria are the “power plants” of cells and are vital for heart function. When these tiny structures are overwhelmed by oxidative stress and calcium overload, they trigger a cascade of damage that weakens heart muscle cells and eventually leads to disease.
Mitochondria under Attack in Heart Disease
The heart is a high-energy organ, and its cells depend on mitochondria to generate ATP, the fuel needed for contraction. Under normal conditions, mitochondria also regulate calcium levels to maintain cellular balance. But during disease states, calcium accumulates excessively in the mitochondria, which not only hampers energy production but also leads to the creation of harmful ROS like superoxide and hydrogen peroxide. These ROS attack cell components—lipids, proteins, DNA—causing widespread damage and eventually cell death.
As the study shows, oxidative stress is worsened by reduced activity of the body’s own antioxidant systems such as catalase, superoxide dismutase, and glutathione peroxidase. The result is an environment where ROS levels spiral out of control, damaging the mitochondrial membrane and opening channels that release death-inducing proteins like cytochrome C into the cell.
Chain Reaction of Cellular Destruction
One of the most alarming findings of the study was the self-perpetuating cycle between oxidative stress and calcium overload. Elevated ROS leads to increased mitochondrial calcium uptake, and the more calcium that enters the mitochondria, the more ROS is generated—a vicious cycle that amplifies cellular injury.
This cycle also disrupts the mitochondrial permeability transition pore (MPTP), which when opened permanently, leads to the loss of mitochondrial membrane potential, ATP depletion, and irreversible cell death. Notably, changes in these processes were observed not just in experimental models but also in failing human hearts, indicating a clear relevance to human disease.
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The Role of Metabolism and Mitochondrial Shape
The research also showed how chronic conditions like diabetes shift the heart’s metabolism from using glucose to burning fat. While fats produce more energy, they require more oxygen and generate more ROS, placing even more stress on already weakened mitochondria. Moreover, the physical structure of mitochondria—controlled by fusion and fission proteins—becomes altered, leading to fragmented, dysfunctional organelles.
In diabetic hearts, for instance, certain proteins that regulate calcium transport like MICU1 become overexpressed while essential calcium channels are downregulated, impairing mitochondrial function even further. These changes not only reduce the heart’s energy supply but also increase its susceptibility to arrhythmias and cell death.
Hope for New Treatments
Encouragingly, the study highlighted possible therapeutic strategies. By restoring mitochondrial calcium balance, boosting antioxidant defenses, or targeting the MPTP to prevent it from opening, it may be possible to prevent or slow down heart damage. Drugs like diazoxide that open mitochondrial potassium channels or agents like cyclosporine A that inhibit MPTP opening have shown promise. Even lifestyle factors, including circadian rhythm regulation and diet, may influence mitochondrial health.
Conclusion
This extensive review has clearly established that mitochondrial dysfunction and oxidative stress are not just byproducts of heart disease but are active drivers of its progression. When mitochondria are overwhelmed by calcium and ROS, energy production fails, cells die, and heart function declines. These discoveries offer a critical understanding of how the heart breaks down at the cellular level and highlight new paths for early intervention. Protecting mitochondrial health could soon become a cornerstone of heart disease prevention and therapy. Developing novel treatments that target mitochondrial ROS production, stabilize calcium handling, and prevent apoptotic signaling could significantly improve outcomes for millions of people affected by cardiovascular disease.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.preprints.org/manuscript/202504.0012/v1
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