Mitochondrial 'Circuit Breaker' Protects Heart from Damage6 years, 1 month ago
Posted on Apr 21, 2017, 6 a.m.
Heart mitochondria build power grid networks that enable them to limit disturbances in energy flow to a smaller region, preventing damage to an entire muscle
Scientists have discovered biological mechanisms that protect the hearts power grid. One of the mechanisms functions like a circuit breaker allowing energy to keep flowing to the heart cells. This power grid is a network of mitochondrial circuits inside heart muscle cells that can keep on functioning even though individual components of those cells, the mitochondria, are damaged.
Researchers wanted to study these protective mechanisms to understand how skeletal and heart muscles function in healthy people and those with mitochondrial diseases, heart disease, and muscular dystrophy. The team of researchers from the National Institutes of Health released their study to the journal Cell Reports.
In 2015, the same research team discovered the mitochondrial power grid in human skeletal muscles. Even though questions were raised by other scientists who were skeptical of how this power grid actually worked, the study did reveal some key observations.
The scientists used 3D images to better see what makes up the hearts power grid. What they saw was a system of mitochondrial circuits throughout the heart. This system offered protection to the power grid if there was any disease-related damage. The mitochondrial circuits were organized in parallel rows of sub-networks, which differed from skeletal muscles which are organized in a single large network. The mitochondrial sub-networks limit electrical dysfunction spreading to smaller areas, which act like a mechanism preventing any damage.
The circuit breaker mechanism in the heart can be compared to a city power grid. If enough lightning were to strike the city the circuit breakers would activate, preventing total power loss to the city. This appears to be how the biological power grid protects the heart from damage.
Cell Reports (2017). DOI: 10.1016/j.celrep.2017.03.063