Mitochondria carry multiple copies of their own genome organized into nucleoids, which include the nuclear-encoded DNA polymerase γ (POLG) and transcription factor A (TFAM)
19. TFAM also helps maintaining mitochondrial DNA (mtDNA) integrity. We previously reported that
H.
pylori induces mtDNA mutations in gastric epithelial cells, also observed in gastritis patients, indicating an early occurrence of mtDNA instability during disease progression
20.
H.
pylori also impairs mtDNA repair pathways.
Mitochondria are essential organelles not only responsible for energy production but also involved in apoptosis, calcium homeostasis, lipids and amino acids metabolism. Targeting mitochondria has emerged as a key strategy for bacteria to hijack host cells physiology and promote infection
1,
2. However, the underlying mechanisms and their relevance to disease remain to a great extent unresolved. Virulence factors of both intracellular and extracellular bacteria are secreted in the host cells and may interact with mitochondria, leading to modulation of mitochondrial function and ultimately promoting pathogenesis
3,
4,
5. Mitochondria have also been reported as modulators of cellular antibacterial immunity and inflammatory response
6.
Helicobacter pylori is a human gastric pathogen and a major risk factor for gastric cancer
7,
8.
H.
pylori damages gastric cells introducing genetic instability and mitochondrial dysfunction, which largely contribute to the infection-associated pathogenicity
9,
10,
11,
12.
Mitochondria carry multiple copies of their own genome organized into nucleoids, which include the nuclear-encoded DNA polymerase γ (POLG) and transcription factor A (TFAM)
19. TFAM also helps maintaining mitochondrial DNA (mtDNA) integrity. We previously reported that
H.
pylori induces mtDNA mutations in gastric epithelial cells, also observed in gastritis patients, indicating an early occurrence of mtDNA instability during disease progression
20.
H.
pylori also impairs mtDNA repair pathways
21.
