Mitochondria are double-membrane organelles that play a role in ATP synthesis, calcium homeostasis, oxidation-reduction status, apoptosis, and inflammation. Several human disorders have been linked to mitochondrial dysfunction. It has been found that traditional therapeutic herbs are effective on alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) which are leading causes of liver cirrhosis and hepatocellular carcinoma. The generation of reactive oxygen species (ROS) in response to oxidative stress is caused by mitochondrial dysfunction and is considered critical for treatment. The role of oxidative stress, lipid toxicity, and inflammation in NAFLD are well known. NAFLD is a chronic liver disease that commonly progresses to cirrhosis and chronic liver disease, and people with obesity, insulin resistance, diabetes, hyperlipidemia, and hypertension are at a higher risk of developing NAFLD. NAFLD is associated with a number of pathological factors, including insulin resistance, lipid metabolic dysfunction, oxidative stress, inflammation, apoptosis, and fibrosis. As a result, the improvement in steatosis and inflammation is enough to entice researchers to look into liver disease treatment. However, antioxidant treatment has not been very effective for liver disease. Additionally, it has been suggested that the beneficial effects of herbal medicines on immunity and inflammation are governed by various mechanisms for lipid metabolism and inflammation control. This review provided a summary of research on herbal medicines for the therapeutic implementation of mitochondria-mediated ROS production in liver disease as well as clinical applications through herbal medicine. In addition, the pathophysiology of common liver disorders such as ALD and NAFLD would be investigated in the role that mitochondria play in the process to open new therapeutic avenues in the management of patients with liver disease.

Cancer cell plasticity drives metastasis and therapy resistance through dynamic transitions between epithelial, mesenchymal, and neural crest stem-like (NCSC) states; however, a unifying mechanism that stabilizes these transitions remains undefined. To address this gap, we introduce a N-cadherin (CDH2)-centered redox–adhesion–exosome (RAX) hub that links oxidative signaling, adhesion dynamics, and exosome-mediated immune communication into a closed-loop framework. Within this network, reactive oxygen species (ROS) pulses license epithelial–mesenchymal transition (EMT), AXL–FAK/Src signaling consolidates mesenchymal adhesion, and selective exosomal cargoes—including miR-21, miR-200, miR-210, and PD-L1—propagate plasticity and immune evasion. Lipid peroxidation acts as a central checkpoint connecting ROS metabolism to PUFA membrane remodeling and ferroptosis vulnerability, buffered by NRF2–GPX4 and FSP1/DHODH axes, thereby converting transient oxidative pulses into persistent malignant states. Mechanistically, the RAX hub synthesizes findings from EMT/CSC biology, ferroptosis defenses, and exosome research into a self-reinforcing system that sustains tumor heterogeneity and stress resilience. Evidence from single-cell and spatial transcriptomics, intravital ROS imaging, and exosome cargo-selector studies supports the feasibility of this model. We further outline validation strategies employing HyPer–EMT–CDH2 tri-reporters, CRISPR perturbation of YBX1/ALIX cargo selectors, and spatial multi-omics in EMT-high tumors. Clinically, tumors enriched in EMT/NCSC programs—such as melanoma, neuroblastoma, small-cell lung cancer, pancreatic ductal adenocarcinoma, and triple-negative breast cancer (TNBC)—represent RAX-dependent contexts. These insights highlight biomarker-guided opportunities to target adhesion switches, ferroptosis defenses, and exosome biogenesis through lipid peroxidation-centered strategies using liquid-biopsy panels (exosomal CDH2, miR-200, miR-210) combined with organoid and xenograft models. By linking lipid peroxidation to ferroptosis defense and oxidative stress adaptation, the RAX hub aligns with the thematic focus of lipid metabolism and redox control in cancer progression. Collectively, the RAX framework may provide a conceptual basis for precision oncology by reframing metastasis and therapy resistance as emergent network properties.

Pancreatic cancer (PC) is currently recognized as the seventh most prevalent cause of cancer-related mortality among individuals of both genders. It is projected that a significant number of individuals will succumb to this disease in the forthcoming years. Extensive research and validation have been conducted on both gemcitabine and 5-fluorouracil as viable therapeutic options for PC. Nevertheless, despite concerted attempts to enhance treatment outcomes, PC continues to pose significant challenges in terms of achieving effective treatment alone through chemotherapy. Gallic acid, an endogenous chemical present in various botanical preparations, has attracted considerable attention due to its potential as an anticancer agent. The results of the study demonstrated that gallic acid exerted a decline in cell viability that was dependent on its concentration. Furthermore, it efficiently suppressed cell proliferation in PC cells. This study observed a positive correlation between gallic acid and the production of reactive oxygen species (ROS). Additionally, it confirmed the upregulation of proteins associated with the protein kinase-like endoplasmic reticulum kinase (PERK) pathway, which is one of the pathways involved in endoplasmic reticulum (ER) stress. Moreover, the administration of gallic acid resulted in verified alterations in the transmission of mitogen-activated protein kinase (MAPK) signals. Notably, an elevation in the levels of p-p38, which represents the phosphorylated state of p38 MAPK was detected. The scavenger of reactive oxygen species (ROS), N-Acetyl-L-cysteine (NAC), has shown inhibitory effects on phosphorylated p38 (p-p38), whereas the p38 inhibitor SB203580 inhibited C/EBP homologous protein (CHOP). In both instances, the levels of PARP have been successfully reinstated. In other words, the study discovered a correlation between endoplasmic reticulum stress and the p38 signaling pathway. Consequently, gallic acid induces the activation of both the p38 pathway and the ER stress pathway through the generation of ROS, ultimately resulting in apoptosis. The outcomes of this study provide compelling evidence to support the notion that gallic acid possesses considerable promise as a viable therapeutic intervention for pancreatic cancer.

Saffron (Crocus sativus L.), known as the world’s most valuable spice, has long been appreciated for its culinary, medicinal, and cultural significance. In recent years, increasing scientific attention has been directed toward its unique phytochemical profile and wide-ranging therapeutic potential. This review provides a comprehensive synthesis of current evidence regarding saffron’s chemical composition, molecular mechanisms of action, pharmacological activities, and safety aspects. The stigmas of saffron contain a rich array of bioactive constituents, notably crocin, crocetin, picrocrocin, and safranal, which collectively contribute to its antioxidant, anti-inflammatory, immunomodulatory, cardioprotective, hepatoprotective, neuroprotective, anti-obesity, antidiabetic, and anticancer properties. Evidence from in vitro and in vivo models, as well as clinical studies, suggests that saffron primarily exerts its beneficial effects through the modulation of oxidative stress, apoptosis, autophagy, lipid metabolism, and the regulation of key molecular pathways, including the NF-κB, PI3K/Akt/mTOR, and Nrf2/HO-1 pathways. Furthermore, recent advances in nanotechnology-based formulations have demonstrated improved bioavailability and enhanced therapeutic efficacy, thereby opening up promising avenues for clinical applications. While saffron is generally regarded as safe, challenges remain concerning its high cost, limited availability, and variability in quality due to geographic and environmental factors. Collectively, the accumulated body of evidence highlights saffron as a promising natural agent for the prevention and management of chronic diseases. However, further translational and large-scale clinical investigations are needed to fully establish its therapeutic value and optimize its integration into modern pharmacological and nutraceutical strategies.

Glioblastoma (GB) remains a major challenge owing to its extremely aggressive nature and resistance to conventional therapies. This review focuses on the intricate roles of progenitor cells, microglia, and non-coding RNAs (ncRNAs) in orchestrating GB pathogenesis and therapy resistance. Glioma stem cells (GSCs), derived from progenitor cells, are important drivers of tumor initiation and recurrence and exhibit remarkable plasticity and resistance to treatment. Microglia, the immune cells of the brain, are hijacked by GB cells to create an immunosuppressive microenvironment that supports tumor growth and resistance to therapy. Non-coding RNAs, including microRNAs and long noncoding RNAs, regulate multiple resistance mechanisms by modulating gene expression and influencing the interactions between progenitor cells and microglia. This review highlights new insights into these interconnected signaling pathways and explores potential therapeutic strategies targeting these molecular players to overcome treatment resistance and improve outcomes in patients with GB.

The combined use of Zingiber officinale (ginger) and Citrus limon (lemon) has long been valued in traditional medicine for their significant therapeutic properties, particularly in supporting cardiovascular health. However, their synergistic effects on hyperlipidemia and oxidative stress, both critical risk factors for cardiovascular diseases, remain underexplored. This study employed a multidisciplinary approach including in vivo (mice model with triton WR-1339-induced hyperlipidemia), in vitro (antioxidant assays such as DPPH and ABTS), and in silico (molecular docking targeting HMG-CoA reductase) to evaluate the hypolipidemic and antioxidant potential of ginger and lemon juices. Phytochemical analysis identified high concentrations of bioactive compounds, with ginger juice containing 6-gingerol (15.54% peak area) and lemon juice featuring hesperidin (13.85% peak area) and rutin (5.57% peak area). These compounds were instrumental in the observed pharmacological effects. The combined formulation significantly improved lipid profiles, reducing total cholesterol by 54.3%, triglycerides by 49.8%, and LDL by 58.1% while increasing HDL by 47.6% compared to hyperlipidemic controls (p < 0.05). Antioxidant assays revealed high free radical scavenging activity, with IC ₅₀ values of 30.92 ± 2.00 µg/mL for ABTS and 44.94 ± 1.02 µg/mL for DPPH in the combined formulation. Molecular docking confirmed strong binding affinities, with hesperidin and 6-gingerol showing binding energies of -10.4 kcal/mol and -9.6 kcal/mol, respectively, against HMG-CoA reductase. In conclusion, combining Zingiber officinale and Citrus limon juices demonstrates robust hypolipidemic and antioxidant effects, significantly outperforming the individual juices. These results support their potential as natural therapeutic agents for managing hyperlipidemia and oxidative stress. Further clinical studies are recommended to validate these promising findings and explore their application in nutraceutical development.