Influenza virus infection (IVI): IVI is one of critical global health issues, which may cause the yearly and sporadic pandemic [1, 2]. IVI approximately costs on $71-167 billion per year in United States [3]. Influenza viruses are classified to RNA viruses and have three subunits; Influenza virus A, B and C. Type A viruses are mostly associated in human disease and are divided into subtypes depends on hemagglutinin (HA) and neuraminidase (NA) serotype [1]. In lung disease, IVI exacerbates asthma, acute lung injury and COPD pathogenesis and also triggers pulmonary fibrosis during the recovery phase [4]. Especially, IVI poses severe health problem to infants, elderly and immunocompromised people [5]. To prevent the influenza infection and pandemics,
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Electron transfer chain (ETC) is the key reactions which take place at mitochondrial cristae, which facilitates proton gradient to generate ATP [8]. Mitochondrial is responsible for generating over 90 % of the energy which is required to maintain the body system [8]. This respiration processes are regulated by several subunits which are encoded in nuclear (~77) and mitochondrial (13) genes [9]. Defect or depletion of mitochondrial respiration stimulates cell death pathway which damages brain, heart, liver, skeletal muscles, kidney endocrine and even respiratory systems [10, 11]. Immunologically, mitochondrial respiration is critical in T cells activation and CD8 T cell memory development, B cells lymphoma development, M1 macrophages differentiation and macrophage phagocytosis [12, 13]. Mitochondrial respiration and its dysregulation were closely related to oxidative stress, which are associated with asthma, COPD, cystic fibrosis and acute respiratory distress syndrome (ARDS) [14]. And viral infection causes mitochondrial dysregulation which is related to development of pulmonary pathogenesis [15]. However, the regulation of mitochondrial respiration by miRNAs is not investigated and the roles in influenza viral infection, either. Therefore, modulation of mitochondrial respiration can be a novel target in IVI research
Electron transfer chain (ETC) is the key reactions which take place at mitochondrial cristae, which facilitates proton gradient to generate ATP [8]. Mitochondrial is responsible for generating over 90 % of the energy which is required to maintain the body system [8]. This respiration processes are regulated by several subunits which are encoded in nuclear (~77) and mitochondrial (13) genes [9]. Defect or depletion of mitochondrial respiration stimulates cell death pathway which damages brain, heart, liver, skeletal muscles, kidney endocrine and even respiratory systems [10, 11]. Immunologically, mitochondrial respiration is critical in T cells activation and CD8 T cell memory development, B cells lymphoma development, M1 macrophages differentiation and macrophage phagocytosis [12, 13]. Mitochondrial respiration and its dysregulation were closely related to oxidative stress, which are associated with asthma, COPD, cystic fibrosis and acute respiratory distress syndrome (ARDS) [14]. And viral infection causes mitochondrial dysregulation which is related to development of pulmonary pathogenesis [15]. However, the regulation of mitochondrial respiration by miRNAs is not investigated and the roles in influenza viral infection, either. Therefore, modulation of mitochondrial respiration can be a novel target in IVI research