Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

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Head and neck squamous cell carcinoma (HNSCC) cells that are positive for human papillomavirus (HPV+) favor mitochondrial metabolism rather than glucose metabolism. However, the involvement of mitochondrial metabolism in HNSCC HPV+ cells is still unknown. The aim of this work was to evaluate the role of E6 oncoproteins from HPV16 and HPV18 in the mitochondrial metabolism in an HNSCC model. We found that E6 from both viral types abates the phosphorylation of protein kinase B-serine 473 (pAkt), which is associated with a shift in mitochondrial metabolism. E6 oncoproteins increased the levels of protein subunits of mitochondrial complexes (I to IV), as well as the ATP synthase and the protein levels of the voltage dependent anion channel (VDAC). Although E6 proteins increased the basal and leak respiration, the ATP-linked respiration was not affected, which resulted in mitochondrial decoupling. This increase in leak respiration was associated to the induction of oxidative stress (OS) in cells expressing E6, as it was observed by the fall in the glutathione/glutathione disulfide (GSH/GSSG) rate and the increase in reactive oxygen species (ROS), carbonylated proteins, and DNA damage. Taken together, our results suggest that E6 oncoproteins from HPV16 and HPV18 are inducers of mitochondrial metabolism.

Summary While high‐risk human papillomavirus (HR‐HPV) infection is related to the development of cervical, vulvar, anal, penile and oropharyngeal cancer, low‐risk human papillomavirus (LR‐HPV) infection is implicated in about 90% of genital warts, which rarely progress to cancer. The carcinogenic role of HR‐HPV is due to the overexpression of HPV E5, E6 and E7 oncoproteins which target and modify cellular proteins implicated in cell proliferation, apoptosis and immortalization. LR‐HPV proteins also target and modify some of these processes; however, their oncogenic potential is lower than that of HR‐HPV. HR‐HPVs have substantial differences with LR‐HPVs such as viral integration into the cell genome, induction of p53 and retinoblastoma protein degradation, alternative splicing in HR‐HPV E6‐E7 open reading frames, among others. In addition, LR‐HPV can activate the autophagy process in infected cells while HR‐HPV infection deactivates it. However, in cancer HR‐HPV might reactivate autophagy in advance stages. Autophagy is a catabolic process that maintains cell homoeostasis by lysosomal degradation and recycling of damaged macromolecules and organelles; nevertheless, depending upon cellular context autophagy may also induce cell death. Therefore, autophagy can contribute either as a promotor or as a suppressor of tumours. In this review, we focus on the role of HR‐HPV and LR‐HPV in autophagy during viral infection and cancer development. Additionally, we review key regulatory molecules such as microRNAs in HPV present during autophagy, and we emphasize the potential use of cancer treatments associated with autophagy in HPV‐related cancers.

Chronic kidney disease (CKD) is a world health problem increasing dramatically. The onset of CKD is driven by several mechanisms; among them, metabolic reprogramming and changes in redox signaling play critical roles in the advancement of inflammation and the subsequent fibrosis, common pathologies observed in all forms of CKD. Extracellular vesicles (EVs) are cell-derived membrane packages strongly associated with cell-cell communication since they transfer several biomolecules that serve as mediators in redox signaling and metabolic reprogramming in the recipient cells. Recent studies suggest that EVs, especially exosomes, the smallest subtype of EVs, play a fundamental role in spreading renal injury in CKD. Therefore, this review summarizes the current information about EVs and their cargos’ participation in metabolic reprogramming and mitochondrial impairment in CKD and their role in redox signaling changes. Finally, we analyze the effects of these EV-induced changes in the amplification of inflammatory and fibrotic processes in the progression of CKD. Furthermore, the data suggest that the identification of the signaling pathways involved in the release of EVs and their cargo under pathological renal conditions can allow the identification of new possible targets of injury spread, with the goal of preventing CKD progression.

High-risk human papillomavirus (HR-HPV) chronic infection is associated with the induction of different HPV-related cancers, such as cervical, anus, vaginal, vulva, penis and oropharynx. HPV-related cancers have been related to oxidative stress (OS), where OS has a significant role in cancer development and maintenance.Surgical resection is the treatment of choice for localised HPV-related cancers; however, these malignancies commonly progress to metastasis. In advanced stages, systemic therapies are the best option against HPV-related cancers. These therapies include cytokine therapy or a combination of tyrosine kinase inhibitors with immunotherapies. Nevertheless, these strategies are still insufficient. Cell redoxsensitive signalling pathways have been poorly studied, although they have been associated with the development and maintenance of HPV-related cancers. In this review, we analyse the known alterations of the following redox-sensitive molecules and signalling pathways by HR-HPV in HPV-related cancers: MAPKs, Akt/TSC2/ mTORC1, Wnt/β-Cat, NFkB/IkB/NOX2, HIF/VHL/VEGF and mitochondrial signalling pathways as potential targets for redox therapy.