Cholesterol is best known for building up in arteries and increasing the risk of heart attacks and strokes.
But scientists have discovered another way excess cholesterol may harm the heart: it can build up inside the tiny structures that supply heart cells with energy.
An international research team led by Dr. Vicenta Llorente-Cortés at the Institute of Biomedical Research of Barcelona found that cholesterol can accumulate inside mitochondria in heart muscle cells. The researchers also tested an experimental antibody treatment that helped reverse some of this damage in an animal model.
The findings were published in the Journal of Lipid Research. The study provides a new look at how cholesterol may contribute to heart problems beyond its well-known effects on blood vessels.
Mitochondria are often described as the powerhouses of cells because they turn nutrients into usable energy. They are especially important in the heart, which must contract continuously to pump blood around the body.
Heart muscle cells contain unusually large numbers of mitochondria because they need so much energy. These structures produce ATP, a molecule that acts as the main energy source for many cellular activities, including the repeated contractions of heart muscle.
The researchers found that cholesterol stored as cholesteryl esters could accumulate in heart-cell mitochondria. As this happened, the mitochondria became damaged and were less able to produce energy efficiently.
A protein called LRP1 appears to play an important role in this process. LRP1 is found on the surface of heart cells and helps move certain fats and cholesterol-carrying particles into the cells.
Under conditions linked to high cardiovascular risk, including high cholesterol, obesity and diabetes, more cholesterol may enter heart cells through this pathway. The researchers found that some of this cholesterol can eventually reach the mitochondria and interfere with their normal function.
This could be important because a heart that cannot produce enough energy may gradually become weaker. Poor mitochondrial function has already been linked to several forms of heart disease and heart failure.
The team then investigated whether blocking part of the LRP1 pathway could protect the mitochondria. They developed monoclonal antibodies that target a specific section of LRP1 known as the P3 domain.
Monoclonal antibodies are laboratory-made proteins designed to attach to a particular target. In this case, the experimental antibodies were intended to interfere with the pathway that allows harmful cholesterol buildup inside heart cells.
The treatment was tested in rabbits with cholesterol patterns that researchers considered useful for studying human cardiovascular disease. Scientists examined the animals’ heart tissue using methods that allowed them to measure energy production, identify fats and closely inspect mitochondrial structure.
After treatment with the antibodies, the researchers found less cholesterol inside the mitochondria. The mitochondria also showed improvements in their internal structure, including the folds known as cristae that are essential for efficient energy production.
The treatment improved the process mitochondria use to make ATP. It also appeared to improve communication between mitochondria and lipid droplets, which are structures that store fats inside cells and help regulate how those fats are used.
These results suggest that protecting mitochondria from excess cholesterol could become a new way of treating some forms of heart disease. Instead of focusing only on cholesterol circulating in the bloodstream, future treatments might also protect the heart from damage occurring inside its own cells.
That would represent a different approach from many existing treatments. Current therapies can lower blood cholesterol, reduce blood pressure and decrease the heart’s workload, but they do not specifically remove cholesterol that has accumulated inside heart-cell mitochondria.
However, the antibody therapy remains experimental. The results came from laboratory and animal research, so scientists still need to determine whether the same approach is safe and effective in people.
Further studies will also need to examine possible side effects and determine which patients might benefit most. Treatments that interfere with important cell receptors must be carefully tested because those receptors can have several jobs throughout the body.
Even so, the research identifies a previously underappreciated connection between cholesterol and the heart’s energy system. If future human studies confirm the findings, protecting mitochondria could eventually become another tool for preventing or treating heart damage in people at high cardiovascular risk.
The research was led by Dr. Vicenta Llorente-Cortés and published in the Journal of Lipid Research.
If you care about heart health, please read studies about top 10 foods for a healthy heart, and how to eat right for heart rhythm disorders.
For more health information, please see recent studies about how to eat your way to cleaner arteries, and salt and heart health: does less really mean more?
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