Research at Tokyo Medical and Dental University has revealed that oral pathogens Porphyromonas gingivalis It may interfere with the repair of the heart muscle after a heart attack, suggesting that treating oral infections may help prevent fatal heart attacks.
Scientists at Tokyo Medical and Dental University have discovered the bacteria that causes periodontal disease. Porphyromonas gingivalis It may interfere with the binding of autophagosomes and lysosomes. This interference worsens the remodeling of heart tissue and increases the risk of heart rupture after a heart attack.
Did you know that regularly brushing and flossing your teeth not only helps keep your smile bright but also protects your heart? Researchers in Japan recently found that oral infections may lead to heartbreak. It was reported that there is.
This research recently International Journal of Oral Sciences The results of a study conducted by Tokyo Medical and Dental University revealed that a common oral pathogen can interfere with the self-repair of heart muscle cells after a heart attack caused by coronary heart disease.
A heart attack occurs when blood flow in the coronary arteries is blocked, resulting in insufficient nutrition and oxygen supply to the heart muscle, and eventually the heart muscle cells die. To prevent this, cardiomyocytes use a process known as autophagy to dispose of damaged cellular components so that they do not cause cardiac dysfunction.
![Dual inhibitory effect of gingipain on both xenophagy and autophagy](https://scitechdaily.com/images/The-Dual-Suppressive-Effect-of-Gingipain-on-Both-Xenophagy-and-Autophagy-777x671.jpg)
Gingipains released by Pg cleave VAMP8 and inhibit autophagy by preventing autophagosome-lysosome fusion, leading to cardiac dysfunction.Credit: Department of Cardiology, Tokyo Medical University
About the main survey results Porphyromonas gingivalis
“Previous research has shown that periodontal pathogens Porphyromonas gingivalis“Myocardial infarction detected at the site of myocardial infarction occlusion may worsen myocardial vulnerability after infarction,” said Yuka Shiheid Watanabe, lead author of the study. “However, the mechanism underlying this effect remained unclear.”
To investigate this, researchers created the following version. P. gingivalis These cells do not express gingipains, the most potent virulence factor. Previous studies have shown that gingipains can inhibit cells from undergoing programmed cell death in response to injury. They then used this bacterium to infect cardiac muscle cells or mice.
Disruption of autophagy and cardiac muscle cell dysfunction
“The results were very clear,” explains corresponding author Yasuhiro Maejima. “The survival rate of cells infected with mutant bacteria lacking gingipains was much higher than that of cells infected with wild-type bacteria. Furthermore, the effects of myocardial infarction were significantly greater in mice infected with wild-type virus. It was serious. P. gingivalis than those infected with the mutant strain. P. gingivalis No pain in the gums. ”
A closer look at this effect showed that gingipains prevent the fusion of two cellular components known as autophagosomes and lysosomes, a process critical to autophagy. In mice, this increased the size of heart muscle cells and accumulated proteins that are normally removed from the cells to protect the heart muscle.
“Our findings show that P. gingivalis When gingipains are produced, autophagosomes accumulate in excess, which can lead to cell dysfunction, cell death, and ultimately cardiac rupture,” says Shihiramichi Watanabe.
given that P. gingivalis It is thought to have a major impact on the ability of the heart muscle itself to become healthy after a heart attack, and treating this common oral infection may help reduce the risk of a fatal heart attack. there is.
Reference: “The periodontal pathogen Porphyromonas gingivalis damages the myocardium after infarction by inhibiting the fusion of autophagosomes and lysosomes” Yuka Shiheido Watanabe, Yasuhiro Maejima, Shun Nakagama, Qing Tao Huang, Written by Natsuko Tamura and Tetsuo Sasano, September 18, 2023, International Journal of Oral Sciences.
DOI: 10.1038/s41368-023-00251-2
This research was funded by the Ministry of Education and the MSD Life Sciences Foundation.