Published: March 18, 2025
Language: Английский
Published: March 18, 2025
Language: Английский
APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(11-12), P. 2025 - 2046
Published: Oct. 7, 2024
Mitochondria dysfunction is implicated in cell death, inflammation, and autoimmunity. During viral infections, some viruses employ different strategies to disrupt mitochondria-dependent apoptosis, while others, including SARS-CoV-2, induce host apoptosis facilitate replication immune system modulation. Given mitochondrial DNAs (mtDNA) role as a pro-inflammatory damage-associated molecular pattern inflammatory diseases, we examined its levels the serum of COVID-19 patients found it be high relative healthy donors. Furthermore, comparison protein profiles between individuals SARS-CoV-2-infected revealed unique bands patients. Using mass spectroscopy, identified over 15 proteins, whose were 4- 780-fold higher. As mtDNA release from mitochondria mediated by oligomeric form mitochondrial-gatekeeper-the voltage-dependent anion-selective channel 1 (VDAC1)-we investigated whether SARS-CoV-2 alters VDAC1 expression. Among three selected small envelope (E), nucleocapsid (N), accessory 3b E-protein induced overexpression, oligomerization, release. Additionally, this led dysfunction, evidenced increased ROS production cytosolic Ca
Language: Английский
Citations
4Published: March 18, 2025
Language: Английский
Citations
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