Cancer stem cells (CSCs) are a self-renewing population often linked to tumor initiation, metastasis, relapse, and resistance to therapy. While bulk tumor cells are often dependent on glycolysis, CSCs demonstrate metabolic plasticity can switch between glycolysis and OXPHOS (oxidative phosphorylation) depending on context. Mitochondria buffer against stress and allow for a metabolic reprogramming towards apoptosis evasiveness, making mitochondrial function crucial to CSC survival. The acquisition of stem-like traits coincides with the rewiring of mitochondrial metabolism, as newly emerging CSCs intermittently upregulate respiration, ROS detoxification, and metabolic plasticity to satisfy cellular demands. Several regulators converge on this mitochondrial metabolism axis. For instance, the co-activator peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and partner estrogen-related receptor α (ERRα) promote mitochondria biogenesis and OXPHOS while promoting tumor sphere formation and expression of stemness genes. Conversely, knockdown of PGC-1α reduces sphere formation and stemness. Similarly, a crucial process - mitophagy via AMP-activated protein kinase (AMPK) and related kinases regulate organelle turnover and quality control to promote CSC viability against stress. Mitochondrial dynamics (fission/fusion) also decides the fate of CSCs. The CSC metabolism is further influenced by the tumor microenvironment (TME). Hypoxia-inducible transcription factors, along with tumor stromal signals such as CAF-derived metabolites induce metabolic rewiring and strengthen antioxidant defenses in CSCs, thereby making it easier for CSCs to survive in unfavourable niches. The abundance of mitochondrial DNA and basal respiratory activity has been linked to CSC features such as increased ATP, stem cell markers and chemoresistance. Over the past few years, significant progress has been made in targeting mitochondrial metabolism of CSCs, yet is still a developing area with tremendous therapeutic scope. More research is required to identify mitochondrial vulnerabilities that are specific to therapy and then translate those findings into effective, precision-based cancer treatments. In this review, we try to provide a comprehensive overview of mitochondrial metabolism in regulating behaviour of CSCs, origin and characteristics of CSCs, the metabolic reprogramming for OXPHOS and glycolytic flexibility, molecular regulators of mitochondrial function, mitochondrial dynamics in stemness pathways and how the TME regulates these processes. We also review novel diagnostic techniques and therapies that target mitochondrial vulnerabilities to eliminate CSCs and provide better clinical outcomes.

Community awareness and rural development play a crucial role in achieving the Sustainable Development Goals (SDGs). To effectively address the global challenges outlined by the SDGs, gathering relevant data and insights at the grassroots is essential. Addressing global problems requires implementing localised solutions tailored to the specific needs of each community, recognizing that these needs vary across different communities. The potential of a flexible real-time geospatial survey platform that helps in finding such solutions is explored here. The geo-tagged empirical data gathered through the platform encompasses infrastructure, socioeconomic, natural resource, and environmental data. Prioritising informed consent and privacy protection, participants are made aware of the purpose of data collection and its use. The example of the N agarcoil Water Survey highlights the collection of data related to water availability, quality, and usage patterns, enabling valuable insights for water resource management. Future improvements may involve incorporating advanced data collection methods, integrating with existing datasets, ensuring data integrity by removal of duplicate and outdated data, and integrating with government portals like Open Government Data and GatiShakti.

Background Sickle Cell Disease (SCD) is a chronic inflammatory disease that is continuously characterized by repeated hemolysis, vaso-occlusive crises (VOC), and chronic low-grade inflammatory state which is caused by the DAMPs released from the damaged red blood cells. Cell-free Mitochondrial DNA (cf-mtDNA) is one of these DAMPs due to its capability of activating the formation of neutrophil extracellular traps for the induction of VOC. However, the inflammatory processes and molecular mechanisms of cf-mtDNA in SCD remain unclear, and it is still unexplored as a potential biomarker especially within sub-Saharan African (SSA) populations. This review tried to synthesize the current information regarding cf-mtDNA in SCD and explore its origin, inflammatory processes, and potential uses as a clinical biomarker. Method The scoping review was conducted according to the Guidelines of the Joanna Briggs Institute Reviewer’s Manual and reported in accordance with PRISMA-ScR guidelines. Searches were done in the databases of MEDLINE/Pubmed, Google Scholar, and Scopus with the keywords "sickle cell", "DAMP", and other inflammatory-associated terms. Out of the 1584 articles searched, only 11 fulfilled the requirements for inclusion. Nine studies were conducted in the US while the remaining two studies came from the Netherlands, while no studies included participants from Africa. Results Evidence suggests that cf-mtDNA might come from retained mature sickle erythrocytes and trigger NET formation through the cGAS-STING-TBK1 pathway. Nevertheless, there is limited direct evidence connecting cf-mtDNA to VOC occurrence, severity and response to treatment. Studies also presented evidence about biomarkers related to whole blood mtDNA counts, deletions and heteroplasmy load being more significant than the evidence related to cf-mtDNA itself. Conclusion The current evidence indicates that cf-mtDNA can be regarded both as a DAMP and a biomarker nonspecifically in regard to SCD, however, clinical relevance is yet to be confirmed. Further longitudinal research is necessary to explore the predictive power of cf-mtDNA for VOCs, severity of the disease and therapy efficacy as well as surface its relation with other inflammatory DAMPs. To solve these gaps in knowledge additional studies among larger cohorts with sufficient geographic diversity especially from SSA are necessary to be conducted.

Over the last three decades, we have witnessed three major outbreaks—SARS, MERS, and COVID-19—resulting in approximately 35 million infections worldwide. SARS-CoV-2, in particular, has developed sophisticated methods to hijack host mechanisms, often involving differentially expressed genes and long non-coding RNAs (lncRNAs), which our lab has studied extensively over the past five years. This study investigates whether the SARS-CoV-2 genome mimics elements of the host genome to facilitate replication, evade the immune system, and hijack host machinery. We achieved this by analyzing sequence similarities between the viral genome and the human genome, including the mitochondrial genome. Our work presents the mechanisms associated with SARS-CoV-2 transgression and explores the plausible implications of lateral gene transfer.