Mitochondrion, Год журнала: 2024, Номер 80, С. 101977 - 101977
Опубликована: Ноя. 4, 2024
Язык: Английский
Journal of Cellular and Molecular Medicine, Год журнала: 2025, Номер 29(3)
Опубликована: Фев. 1, 2025
ABSTRACT Hepatocellular carcinoma (HCC) is a major contributor to cancer‐related deaths globally. Although there have been improvements in identifying treating the disease, patient outcomes are still unfavourable because of significant variation HCC. Mitochondrial‐related genes (MRGs) crucial tumour metabolism, cell death and immune response, emerging as potential therapeutic targets. We analysed 2030 MRGs using TCGA, GEO HCCDB18 databases. Differentially expressed were identified edgeR limma, enrichment analysis was performed via clusterProfiler package. A prognostic model built machine learning algorithms evaluated LOOCV. Immune infiltration assessed with CIBERSORT, EPIC, MCPCounter TIMER algorithms, drug sensitivity CTRP PRISM datasets. MRG expression levels significantly associated worse HCC patients outperformed conventional clinical indicators response revealed that individuals at high risk exhibited weaker responses, characterised by reduced scores, elevated CD8+ T cells macrophages. Notably, high‐risk also displayed heightened susceptibility chemotherapy agents such paclitaxel irinotecan. Abnormal serves biomarker for prognosis. The developed accurately predicts disease progression can guide personalised treatment, especially chemotherapeutic therapies. Further validation broader samples needed.
Язык: Английский
Процитировано
0
Genes, Год журнала: 2025, Номер 16(3), С. 268 - 268
Опубликована: Фев. 25, 2025
The mitochondria–telomere axis is recognized as an important factor in the processes of metabolism, aging and oncogenesis. MicroRNAs (miRNAs) play essential function this complex interaction, having impact on aspects such cellular homeostasis, oxidative responses apoptosis. In recent years, miRNAs have been found to be crucial for telomeric stability, well mitochondrial behavior, factors that influence cell proliferation viability. Furthermore, (mitomiRs) are associated with gene expression activity cGAS/STING pathway activity, linking DNA recognition immune system responses. Hence, maintain a link biogenesis, metabolic changes cancer organelles. This review focuses roles variety progression their potential application biomarkers or therapeutic agents.
Язык: Английский
Процитировано
0
Frontiers in Molecular Neuroscience, Год журнала: 2025, Номер 18
Опубликована: Апрель 1, 2025
Introduction Copper sulfate exposure induces oxidative stress by triggering excessive reactive oxygen species (ROS) production, leading to inflammatory responses, neuroinflammation, and cellular dysfunction. Small humanin-like peptide-6 (SHLP-6), a mitochondria-derived peptide with anti-aging anti-cancer properties, has not been explored for its protective effects against copper toxicity. This study investigates the antioxidant, anti-inflammatory, neuroprotective potential of SHLP-6 in zebrafish larvae exposed sulfate. Methods Zebrafish were treated at concentrations ranging from 10 50 μg/mL. ROS-scavenging activity was assessed using vitro assays, enzymatic antioxidant markers, lipid peroxidation, nitric oxide levels, acetylcholine esterase (AChE) activity, locomotor behavior evaluated. Additionally, gene expression analysis performed markers. Results Treatment 40 μg/mL significantly reduced malformations, improved heart rate (178 bpm), increased survival rates (85%) larvae. The highest ROS inhibition observed 58.7% 74.3%, while enzyme enhanced, superoxide dismutase (68.3 U/mg), catalase (82.40 glutathione (79.3 U/mg). Lipid peroxidation levels decreased 3.86 3.41 U/mg, respectively. AChE (78.3 U/mg) (43.53 m distance travelled). Discussion upregulated TNF-α (2.16-fold), NLRP3 (1.78-fold), COX-2 (0.705-fold), increasing IL-10 (1.84-fold), suggesting neuroinflammation modulation. Antioxidant (SOD, CAT, GST, GSH) upregulated. These findings indicate SHLP-6’s as agent sulfate-induced
Язык: Английский
Процитировано
0
Journal of Controlled Release, Год журнала: 2025, Номер unknown, С. 113720 - 113720
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
0
Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown
Опубликована: Апрель 21, 2025
Abstract Caspase-independent cell death (CICD) has recently become a very important mechanism in lung cancer, particular, to overcome critical failure apoptotic that is common disease progression and treatment failures. The pathways involved CICD span from necroptosis, ferroptosis, mitochondrial dysfunction, autophagy-mediated death. Its potential therapeutic applications have been highlighted. Glutathione peroxidase 4 (GPX4) inhibition-driven ferroptosis drug resistance non-small cancer (NSCLC). In addition, necroptosis involving RIPK1 RIPK3 causes tumor modulation of immune responses the microenvironment (TME). Mitochondrial are for through metabolic redox homeostasis. Ferroptosis amplified by reactive oxygen species (ROS) lipid peroxidation cells, depolarization induces oxidative stress leads mitochondria-mediated autophagy, or mitophagy, results clearance damaged organelles under conditions, while this function also linked when dysregulated. role autophagy regulated ATG proteins PI3K/AKT/mTOR pathway dual: suppress sensitize cells therapy. A promising approach enhancing outcomes involves targeting mechanisms CICD, including inducing SLC7A11 inhibition, modulating ROS generation, combining inhibition with chemotherapy. Here, we review molecular underpinnings particularly on their transform treatment.
Язык: Английский
Процитировано
0
Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Окт. 18, 2024
Breast cancer (BC) remains a significant health issue globally and most common cause of mortality in women. Enhancing our understanding on biomarkers may greatly improve both diagnostic therapeutic approaches to this disease.
Язык: Английский
Процитировано
1
Mitochondrion, Год журнала: 2024, Номер 80, С. 101977 - 101977
Опубликована: Ноя. 4, 2024
Язык: Английский
Процитировано
0