Mitochondrial circuit prevents widespread damage to heart muscle.
Two newly discovered mechanisms of heart cells may result in a better understanding of cardiovascular disease and lead to new treatment options that prevent damage.
The authors of a study published by Cell Reports discovered that these biological mechanisms may prevent damage to the network of mitochondrial circuits that provide energy to the cells.
One mechanism behaves similarly to a circuit breaker by allowing energy to move through the cells even when the mitochondria have sustained damage, according to the study.
These findings could improve the understanding of heart and skeletal muscle function in conditions such as heart disease, mitochondrial disease, and muscular dystrophy.
The authors previously discovered a mitochondrial power grid in skeletal muscle; however, they question how the power grid would protect against muscle cell damage.
In the current study, the authors used 3D images and light-activated probes to determine how the 2-pronged system protects the heart muscle’s mitochondrial power grid against damage.
While the skeletal muscle’s power grid is a large, interconnected network, the heart muscle’s mitochondrial circuit is arranged in parallel rows, according to the study. These rows combine to create multiple smaller subnetworks that protect against damage by limiting the spread of electrical dysfunction.
The authors likened the mitochondrial grid to a bolt of lightning striking a city’s power grid. They wrote that the lights may flicker throughout the city, but once the circuit breaker is on, only a small part loses power. This means that while some portions of the heart may experience dysfunction, the mitochondrial network prevents the damage from spreading.
The mitochondrial power grid was found to be protective against heart disease and could be used to create novel treatments that protect against damage to a variety of muscles, according to the study.
“This mitochondrial network protection system limits the propagation of local failures and allows for the quick recovery of undamaged mitochondria in order to sustain cellular function,” the authors concluded.