@article{Madeddu_Maniga_Zaffanello_Fanos_Marcialis_2022, title={The SARS-CoV2 and mitochondria: the impact on cell fate: SARS-CoV2 and mitochondria}, volume={93}, url={https://mattioli1885journals.com/index.php/actabiomedica/article/view/10327}, DOI={10.23750/abm.v93i2.10327}, abstractNote={<p>Coronavirus infection causes endoplasmic reticulum stress inside the cells, which inhibits protein folding. Prolonged endoplasmic reticulum stress causes an apoptotic process of unfolded protein response-induced cell death. Endoplasmic reticulum stress rapidly induces the activation of mTORC1, responsible for the induction of the IRE1-JNK pathway. IRE1-JNK stands out for its dual nature: pro-apoptotic in the first stage of infection, anti-apoptotic in persistently infected cells. Once penetrated the cells, the virus can deflect the mitochondrial function by implementing both waterfalls pro-apoptotic and anti-apoptotic response. The virus prevents, through Open Reading Frame 9b (ORF-9b) interacting with mitochondria, the response of the type I interferon of the cells affected by the infection and is fundamental for generating an antiviral cellular state. ORF-9b has effects on mitochondrial dynamics, inducing fusion and autophagy and promoting cell survival. The recognition of ORF-9b has made it possible to identify it as a molecular target of some existing potentially effective drugs (Midostaurin and Ruxolitinib). Other drugs, with the same target, are currently being tested. Given the great importance of mitochondria in virus-host interaction, in-depth knowledge of the actors and pathways involved is essential to continue developing new therapeutic strategies against SARS CoV2.</p>}, number={2}, journal={Acta Biomedica Atenei Parmensis}, author={Madeddu, Eleonora and Maniga, Barbara and Zaffanello, Marco and Fanos, Vassilios and Marcialis, Antonietta}, year={2022}, month={May}, pages={e2022199} }