Mitochondria are an important target of photobiomodulation in cardiomyocytes

Photobiomodulation (PBM) has been shown to delay the pathological process of heart failure, but the exact mechanism of action is not clear. Mitochondria occupy one-third of the volume of mammalian cardiomyocytes (CMs) and are central transport stations for CM energy metabolism. Therefore, in this study, we explored the regulatory effects of 630 nm light-emitting diodes (LED-Red) on the mitochondria of CMs. The results show that LED-Red-based PBM promotes adenosine triphosphate (ATP) synthesis by upregulating the expression of glycolipid metabolizing enzymes. Correspondingly, there was an improvement in the activity of succinate dehydrogenase (SDH), a key enzyme in the mitochondrial electron transport chain, and the mitochondrial membrane potential. Meanwhile, LED-Red affected the state of mitochondrial oxidative stress and promoted the generation of reactive oxygen species (ROS), but the increased ROS production did not damage the CMs. In addition, mitochondrial division and fusion were also affected by the stimulation of LED-Red. Finally, PBM treatment led to a significant increase in transcript levels of mitochondrial transcription factor A (TFAM), which controls the stability of the mitochondrial genome. Collectively, irradiation with LEDs at 630 nm played a regulatory role in mitochondrial function, suggesting that mitochondria appear to be the recipients of PBM treatment. This study provides more insights into the mechanisms underlying PBM treatment in heart diseases.