Popovici, IvonaCozma, Andreea-PaulaSolcan, Carmen2026-06-102026-06-1020251454-7406https://repository.iuls.ro/handle/20.500.12811/6597Cellular injury induced by coronaviruses use mitochondria as central targets and regulators. SARS-CoV-2 and related betacoronaviruses disrupt mitochondrial homeostasis through multiple mechanisms, including direct localization of viral proteins to mitochondria, inhibition of oxidative phosphorylation (OXPHOS), excessive reactive oxygen species (ROS) production, altered mitochondrial dynamics, and the release of mitochondrial DNA (mtDNA). These modifications have as a result the reprogram of cellular metabolism, lead to innate antiviral signaling, and activate various programmed cell death pathways, exacerbating inflammatory responses and contributing to disease severity. Mitochondrial dysfunction is considered a critical factor in coronavirus pathogenesis. Elucidating the interplay between coronaviruses and mitochondria is essential for understanding coronaviruses pathogenesis and developing new ways for prevention and therapy.EnglishAttribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)http://creativecommons.org/licenses/by-nc-sa/4.0/coronavirusmitochondriacellular stressArticle2393-4603https://doi.org/10.61900/SPJVS.2025.04.10