Search Results (676)

Type 2 diabetes mellitus is a relevant cardio–renal–metabolic disorder in which chronic low-grade inflammation and oxidative stress have a crucial function in linking insulin resistance, endothelial dysfunction, β-cell impairment, and progressive organ injury. In this context, nutrition has emerged as a key modifiable determinant of metabolic homeostasis, capable of influencing inflammatory signalling, redox balance, mitochondrial function, and gut microbiota–host interactions. The objective of this review is to critically summarise the mechanistic connections among inflammation, oxidative stress, and diabetes progression, and to investigate how dietary factors and patterns, as well as nutrition-responsive biomarkers, influence these pathways and their cardiorenal consequences. We discuss the effects of macronutrient quality, dietary fibre, fatty acids, polyphenols, and specific micronutrients, including vitamin C, vitamin E, selenium, zinc, and magnesium, as well as the role of Mediterranean, DASH, and plant-based diets in improving glycaemic control, endothelial function, and cardio-renal risk profiles. We also summarise established and emerging biomarkers of inflammation and oxidative stress that may improve risk stratification and the evaluation of nutrition-based interventions. Overall, current evidence supports a shift from a purely glucose-centred approach toward an integrated model in which dietary modulation of inflammatory and oxidative pathways helps reduce cardiovascular and renal risk. However, heterogeneity of interventions, variability in biomarker assessment, and interindividual differences in dietary response represent major limitations. Future research should focus on biomarker-informed, precision-oriented nutritional approaches integrated within contemporary cardio–renal–metabolic care. Full article

Objectives: Myelodysplastic syndromes (MDSs) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis, genomic instability, and a high risk of progression to acute myeloid leukemia. Oxidative stress (OS) has emerged as a central factor in MDS pathophysiology, contributing to DNA damage, altered cellular signaling, and disease progression. Recent advances in artificial intelligence (AI) and machine learning (ML) offer a transformative approach for integrating multidimensional datasets including oxidative stress markers, hematologic parameters, and molecular profiles to enhance diagnosis, prognostication, and therapeutic monitoring in MDS. Methods: A comprehensive literature search was conducted in PubMed and Scopus, using the keywords “OS biomarkers,” “AI,” and “MDS’’. Results: Modified redox biomarkers can be correlated with oxidative imbalance and disease progression. ML models such as neural networks, decision trees, and support vector machines effectively capture complex relationships among redox biomarkers, enhancing risk stratification and prediction of treatment response. AI-driven proteomic analyses further revealed OS-related protein signatures linked to MDS pathophysiology. Overall, AI and ML enable the transformation of multidimensional OS data into clinically actionable tools for personalized management in MDS. Conclusions: Integrating biomarker research with AI-based analytics holds promise for advancing personalized diagnostics, prognostication, and therapeutic strategies in MDS, paving the way toward precision medicine. Full article

Polycyclic aromatic hydrocarbons (PAHs) are common environmental contaminants formed during the incomplete combustion of organic material. Their persistence, bioaccumulation, and metabolic activation contribute to mutagenic and cytotoxic outcomes. Among these are benzo[a]pyrene (B[a]P), the most studied PAH and a benchmark compound for PAH carcinogenicity, and pyrene, a PAH whose urinary metabolite 1-hydroxypyrene is widely used as a biomarker of PAH exposure. B[a]P undergoes CYP1A1-mediated oxidation to generate reactive oxygen species (ROS) via epoxide and quinone redox cycling, whereas pyrene produces ROS primarily through pyrene-quinone redox cycling. We investigated cobinamide, a vitamin B₁₂/cobalamin analog with potent antioxidant properties, for mitigating benzo[a]pyrene- and pyrene-induced injury. In H9C2 rat embryonic cardiomyoblasts and A549 human lung epithelial cells exposed to B[a]P (10 μM) or pyrene (10–100 μM), cobinamide (5–10 μM) attenuated PAH-induced reductions in cell number in both models, while in H9C2 cells, it also attenuated decreases in metabolic activity and reduced apoptosis. Cobinamide also returned JNK/p38 phosphorylation to near baseline levels, decreased DNA and protein oxidation and DNA strand breaks. Transcriptionally, cobinamide suppressed inflammatory (TNF-α, IL-1β, and IL-6) and oxidative stress genes (HMOX1 and NOX4), while enhancing oxidative response (SOD2) and xenobiotic metabolism (CYP1A1). In Drosophila melanogaster exposed to 5 mM B[a]P/pyrene, 2 mM cobinamide improved survival and fully restored locomotion, outperforming cobalamin (minimal benefit) and N-acetylcysteine (partial rescue). Spectroscopic analyses showed no direct cobinamide-PAH binding. These findings demonstrate that cobinamide efficiently limits ROS-mediated PAH injury through redox modulation while preserving xenobiotic metabolism, suggesting its potential therapeutic use to mitigate PAH-induced toxicity. Full article

Oxidative stress and inflammation are key drivers of kidney injury and disease progression. In this context, the role of sialic acids emerged as a critical regulatory layer linking redox imbalance, immune activation, and tissue damage. Sialic acids are terminal negatively charged residues that regulate complement activity, immune cell signaling, and the structural integrity of the glomerular filtration barrier. Alterations in sialylation, resulting from impaired biosynthesis or increased sialidase activity, disrupt immune homeostasis, enhance inflammatory responses, and promote complement-mediated injury. In the kidney, these mechanisms contribute to podocyte dysfunction, glomerular inflammation, and fibrosis and are implicated in glomerulopathies, transplantation, and plasma cell dyscrasias. Emerging evidence also highlights the therapeutic potential of targeting sialic acid metabolism through inhibition of desialylation or restoration of sialylation pathways. Overall, sialic acids represent dynamic modulators at the intersection of oxidative stress and immunity, offering novel opportunities for biomarker development and mechanism-based therapies in kidney disease. Full article

Oxidative stress is an important component of cancer biology and is characterized by an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems. Excess ROS can cause molecular damage and genomic instability; at the same time, ROS signaling remains necessary for normal cellular function. Redox homeostasis is of particular importance in this balance. The aim of this structured narrative review was to summarize and critically discuss current evidence on how dietary antioxidants influence redox-sensitive pathways involved in cancer prevention, with particular attention to metabolic inflammation, mitochondrial quality control, and gut microbiota-related mechanisms. We performed a structured literature search of Scopus, Web of Science, and PubMed, focusing on articles published between 2021 and 2026. The evidence covered major redox-sensitive pathways, including Nrf2-Keap1-ARE signaling, AMPK-mTOR regulation, NF-κB-mediated inflammation, mitochondrial quality control (autophagy and mitophagy), and inflammasome activation. These pathways, which are involved in tumor initiation and progression, link oxidative stress to metabolic and inflammatory processes. Current evidence suggests that dietary antioxidants act primarily by supporting endogenous defense systems. This may help explain the “antioxidant paradox”, in which antioxidant-rich dietary patterns are associated with a lower risk of cancer. In some studies, high-dose supplementation with isolated antioxidants has produced inconsistent or sometimes adverse results. These effects depend on dose, chemical form, metabolic context, and baseline redox state. The gut microbiota is also an important mediator of antioxidant bioactivity; by converting dietary polyphenols into bioactive metabolites, it can influence systemic redox balance and metabolic signaling. This microbiota-dependent modulation may partially explain inter-individual variability in responses to dietary interventions. In conclusion, dietary antioxidants should be considered as modulators of redox-sensitive signaling networks, not merely as simple radical scavengers. Personalized modulation of redox homeostasis is a future strategy for cancer prevention, with a greater emphasis on whole-diet and biomarker-guided approaches. Full article

Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in which dopaminergic dysfunction plays a central role. Beyond its neurotransmitter function, dopamine is a redox-active molecule capable of generating reactive oxygen species and toxic intermediates, particularly when cytosolic dopamine accumulates because of altered vesicular storage or transporter imbalance. This review examines whether dopamine-derived oxidative stress may represent a biologically plausible and testable framework for ADHD by integrating current evidence on dopamine metabolism, oxidative stress, and neuronal dysfunction, while distinguishing direct evidence from indirect and translational findings. A structured literature search was conducted in PubMed, Scopus, and Web of Science for relevant English-language studies published between January 2000 and March 2026. The available evidence suggests that dopamine-derived oxidative stress may help link disturbed dopamine handling to protein modification, lipid peroxidation, mitochondrial dysfunction, synaptic inefficiency, and circuit-level abnormalities in ADHD. Although direct in vivo evidence remains limited, this framework may help distinguish dopamine-derived oxidative stress from more general oxidative imbalance in ADHD and may guide future biomarker-based, experimental, and translational research. Full article

Radiation-induced trismus (RIT) is a common and function-limiting late complication of radiotherapy for head and neck cancers, particularly when the masticatory muscles and temporomandibular joint receive high doses. Despite advances in intensity-modulated radiotherapy, RIT remains a significant survivorship problem, and robust biological biomarkers capable of predicting individual susceptibility are lacking. Heat shock protein 27 (HSP27; HSPB1) is a small heat shock protein that regulates multiple cellular stress responses, including proteostasis, cytoskeletal dynamics, redox homeostasis, apoptosis, and inflammatory signaling. In head and neck malignancies, HSP27 overexpression has been associated with treatment resistance and fibrosis-prone tissue remodeling. Experimental studies further demonstrate that HSP27 promotes transforming growth factor-β-mediated myofibroblast differentiation and extracellular matrix deposition, whereas pharmacologic or genetic inhibition attenuates radiation- or bleomycin-induced pulmonary fibrosis in vivo. Evidence from skeletal muscle biology also indicates that HSP27 modulates muscle integrity, denervation-associated atrophy, inflammatory signaling, and cytoskeletal stability. Although HSP27 has been widely investigated in radiation responses, fibrosis, and skeletal muscle stress adaptation, its potential involvement in the pathogenesis of RIT has not been systematically examined. This review proposes a conceptual framework in which HSP27 functions as an integrative molecular mediator linking radiation-induced oxidative stress, endothelial injury, and fibro-atrophic remodeling within the masticatory apparatus. By integrating current evidence on the epidemiology, dosimetric determinants, imaging correlates, and pathophysiology of RIT with the structural and functional biology of HSP27, this review provides the first tissue-specific synthesis of molecular stress signaling and clinical mechanisms relevant to RIT susceptibility. We further suggest that HSP27 signaling may influence susceptibility to fibro-neuromuscular injury in irradiated masticatory tissues. Given the absence of direct experimental or clinical evidence in this setting, these considerations are derived from mechanistic convergence across related biological systems and should be interpreted as biologically plausible but unproven, with potential implications for future biomarker development and biologically informed prevention strategies. Full article

Plastic-derived chemical additives, including bisphenols, phthalates, perfluoroalkyl substances (PFAS) and microplastic-associated contaminants, are now recognised as widespread environmental toxins that measurably affect endocrine signalling, oxidative balance, inflammation and metabolic homeostasis. Continuous exposure through food contact materials, consumer products, and environmental media raises concerns about long-term health effects. An increasing number of epidemiological and experimental studies are linking these exposures to metabolic disorders, reproductive dysfunction, neurodevelopmental alterations, and increased disease susceptibility throughout the lifespan. This narrative review summarises the latest evidence on the toxicological mechanisms of these compounds, with a focus on endocrine disruption, redox imbalance, reproductive impairment, thyroid hormone dysregulation and epigenetic modifications induced by plastic-derived chemicals. Literature was identified through searches of major scientific databases, including PubMed, Scopus, and Web of Science. Reference screening was also employed to complement these searches and ensure comprehensive coverage of vertebrate and invertebrate models. The inclusion criteria encompassed studies published within the last 10 years, focusing on experimental, experimental, and translational research. The review evaluates phytochemicals such as polyphenols, flavonoids, isoflavones, catechins, sulforaphane, and chlorogenic acid as natural agents that can mitigate the biological effects of plastic-derived toxicants. These compounds exhibit antioxidant, anti-inflammatory, and receptor-modulating properties that counteract pathways disrupted by BPA, phthalates, and PFAS. Experimental studies have demonstrated that phytochemicals can modulate oestrogen receptor activity, enhance detoxification systems, reduce oxidative biomarkers and mitigate epigenetic and metabolic alterations induced by micro- and nanoplastics. Emerging nutritional evidence suggests that diets high in polyphenols may reduce the biological impact of plastic-derived contaminants within the body, rather than reducing exposure itself. This effect appears to be especially relevant during sensitive developmental periods, such as the prenatal, early postnatal and adolescent stages. Full article

Background: Branch retinal vein occlusion (BRVO) represents a segmental retinal ischemic disorder characterized by localized oxidative–inflammatory activation. While redox-driven cytokine responses have been described in central retinal vein occlusion, their role in BRVO-specific macular edema and treatment responsiveness remains unclear. This study investigated whether novel redox-related inflammatory mediators in the aqueous humor are associated with disease severity and structural response to anti-vascular endothelial growth factor (VEGF) therapy in BRVO. Methods: Aqueous humor samples were collected from 30 treatment-naïve patients with BRVO and 19 control patients. Levels of VEGF and the novel redox-related inflammatory factors FMS-related tyrosine kinase 3 ligand (Flt-3L), fractalkine, CXCL-16, and endocan-1 were measured by suspension array, and the severity of macular edema was evaluated by measuring central macular thickness and neurosensory retinal thickness (TNeuro) by spectral-domain optical coherence tomography. Therapeutic response was assessed one month after intravitreal ranibizumab injection (IRI). Results: Aqueous levels of VEGF, Flt-3L, and endocan-1 were significantly higher in the BRVO group, and levels of Flt-3L, CXCL-16, and endocan-1—markers associated with oxidative endothelial damage and leukocyte recruitment—correlated significantly with each other and with aqueous flare values. Notably, baseline Flt-3L levels significantly correlated with the reduction in TNeuro, suggesting that this redox-sensitive signaling molecule is a potential biomarker for treatment sensitivity. Conclusions: These findings suggest that novel inflammatory factors, potentially driven by oxidative-nitrosative stress, play a pivotal role in the pathophysiology of BRVO. Baseline Flt-3L may serve as a predictive biomarker for structural responsiveness to anti-VEGF therapy in BRVO, suggesting that oxidative–inflammatory signaling contributes not only to disease severity but also to therapeutic heterogeneity. Full article

Infertility is a global health problem, with male factors contributing to nearly half of all cases. Up to 30% of male infertility is classified as idiopathic, in part because routine semen analysis does not assess sperm fertilizing competence. Capacitation is a complex process that endows spermatozoa with the competence to fertilize the oocyte, and it depends on oxidant-driven phosphorylation events. These events include increased PKA substrate and tyrosine phosphorylation, which promote hyperactivated motility and the acrosome reaction. These pathways are normally restrained by decapacitation factors that must be relieved in the female reproductive tract before capacitation can proceed. Protein CoAlation is an antioxidant modification of protein thiols through a disulfide bond with coenzyme A (CoASH). We previously detected protein CoAlation in human spermatozoa and observed that its levels decline during capacitation, but its function was unknown. We hypothesized that protein CoAlation functions as a decapacitation mechanism that prevents redox signalling, enabling oxidative activation of phosphorylation events during capacitation. Using spermatozoa from healthy human donors, we leveraged subcellular fractionation, immunocytochemistry, computer-assisted sperm analysis (CASA), and immunoblotting to determine the sperm protein CoAlation profile, assess CoASH biosynthetic enzymes, and test how pharmacological modulation of CoAlation levels influences capacitation. CoAlated proteins were distributed across intracellular sperm compartments, and spermatozoa possess the CoASH biosynthetic enzymes PANK2 and CoASY, indicating an intrinsic capacity for CoAlation. Inhibition of CoASH biosynthesis reduced CoAlation and enhanced PKA substrate phosphorylation, tyrosine phosphorylation, hyperactivated motility, and the progesterone-induced acrosome reaction under capacitating conditions. Pantothenic acid supplementation increased CoAlation and suppressed these processes without impairing viability or baseline motility. These findings indicate that high levels of protein CoAlation in several protein bands are a pre-existing feature of the non-capacitated state that restrains the redox-regulated events of capacitation and that its decline is required to permit sperm capacitation. CoAlation levels may emerge as a biomarker of sperm capacitation and fertilizing competence. Full article

This study developed a two-stage, explainable machine learning framework to predict 18-month MMSE-based cognitive status from baseline multimodal data in community-dwelling older adults in Japan. A hierarchical design was used in which Stage 1 distinguished cognitively Normal participants from those with any abnormality (Possible Mild Cognitive Impairment (MCI) or Impaired), and Stage 2 further separated Possible MCI from Impaired within the abnormal subgroup. Both an Imbalanced-Learn Random Forest and a penalized logistic regression baseline were trained under Leave-One-Out Cross-Validation, yielding fair discrimination in Stage 1 (Random Forest AUC = 0.72, accuracy = 0.71; logistic regression AUC = 0.71, accuracy = 0.76) and apparently strong separability in Stage 2 (Random Forest AUC = 0.95, accuracy = 0.96; logistic regression AUC = 0.82, accuracy = 0.92) in a small sample size with high class imbalance. SHapley Additive exPlanations (SHAP) with TreeExplainer for Random Forest and LinearExplainer for logistic regression were used to identify interpretable biomarkers at each stage though feature attribution. In Stage 1, both models highlighted renal and systemic metabolic markers (e.g., creatinine, uric acid, blood urea nitrogen), amino acid and redox-related metabolites (including D-serine, D-amino acid proportions, L-asparagine, alanine, L-glutamic acid, cysteine, methionine sulfoxide), and wearable-derived activity variability (e.g., fluctuation coefficients and steps per minute), with the Simpson index of gut microbiome diversity also contributing in the logistic model. In Stage 2, the models converged on a distinct signature involving glucose and albumin, uric acid and uridine, choline and carnitine, multiple amino acids (such as phenylalanine, proline, ornithine, tryptophan, threonine, and short-chain amino acids), oxidative/energy markers (niacinamide, methionine, methionine sulfoxide, ergothioneine), hematologic indices, and high-MET activity fluctuation metrics. Collectively, these results support a stage-dependent, multisystem view of cognitive aging in which broad renal–metabolic, amino acid, and behavioral vulnerabilities characterize early abnormality, whereas more pronounced alterations in energy metabolism, nucleotide and choline pathways, oxidative stress, and activity irregularity accompany progression from Possible MCI to Impaired status. By combining routine clinical chemistry, targeted metabolomics, gut microbiome diversity, and wearable-derived behavioral measures within an explainable AI framework, this two-stage approach illustrates a scalable, biologically grounded strategy for stage-aware risk stratification and monitoring of cognitive decline in community settings. Full article

Pressure ulcers are chronic wounds characterized by repeated ischemia–reperfusion injury, persistent inflammation, and redox imbalance, in which excessive production of reactive oxygen species (ROS) contributes to delayed healing. Thus, debridement is an essential therapeutic procedure for removing necrotic tissue and biofilm, thereby reconstructing the wound microenvironment. Recent experimental studies suggest that molecular hydrogen may improve wound healing through attenuation of oxidative stress and modulation of inflammatory responses, while debridement represents a dynamic intervention phase in which redox imbalance may transiently develop. Here, we propose the hypothesis that the use of hydrogen-enriched saline as an irrigation solution during hydrosurgical debridement may attenuate excessive redox imbalance and stabilize the wound microenvironment during this dynamic intervention phase. Such intra-procedural modulation may facilitate the transition from inflammation to the proliferative phase of wound healing, thereby promoting tissue repair. This approach is expected to attenuate the transient oxidative burst following debridement, as reflected by reductions in redox-related biomarkers in the wound environment, including ROS levels and oxidative damage markers such as 8-hydroxy-2′-deoxyguanosine and lipid peroxidation products, with relative decreases in these biomarkers compared with conventional debridement, potentially consistent with reductions observed in preclinical oxidative stress models. These findings are consistent with findings from previous experimental studies demonstrating attenuation of oxidative stress markers following hydrogen administration. This hypothesis introduces a novel therapeutic concept, redox modulation during the debridement process, offering a practical strategy for integrating hydrogen-based therapy into existing wound management without altering current surgical techniques. Full article

Mitochondrial RNA (mtRNA) modifications have emerged as critical regulators of pancreatic β-cell bioenergetics, influencing glucose-stimulated insulin secretion (GSIS) and the early pathogenesis of diabetes mellitus (DM). This review synthesizes current evidence on the diversity, mechanisms, and functional implications of mtRNA modifications—such as N6-methyladenosine (m6A), 5-methylcytosine (m5C), pseudouridine (Ψ), and 5-formylcytosine (f5C)—within β-cell mitochondria. These chemical marks, installed and recognized by specific writer, eraser, and reader proteins, regulate mitochondrial translation, oxidative phosphorylation (OXPHOS) complex assembly, and redox balance. Defects in mtRNA modification machinery, exemplified by β-cell-specific knockout of TFB1M, MRM2, or PUS1, impair ribosome biogenesis, disrupt ATP production, and precipitate insulin secretory failure, as demonstrated in human islets, rodent models, and monogenic diabetes syndromes. Advances in epitranscriptomic mapping technologies—including nanopore direct RNA sequencing, RNA immunoprecipitation (RIP)-seq, and mass spectrometry—have enabled high-resolution profiling of mtRNA modification landscapes under physiological and diabetic conditions, revealing their dynamic regulation in response to metabolic stress. Furthermore, mtRNA modifications interact with environmental stressors, such as oxidative damage and toxic metals, modulating β-cell vulnerability via pathways like the mitochondrial unfolded protein response (UPRmt). Therapeutically, modulation of RNA-modifying enzymes or restoration of specific chemical marks holds promise for preserving β-cell function, with potential applications in early diagnosis, risk stratification, and precision medicine approaches for DM. Despite substantial progress, critical gaps remain in understanding the interplay between mtRNA modifications, mitochondrial-nuclear crosstalk, and β-cell plasticity. Addressing these gaps will be pivotal for translating mtRNA biology into novel biomarkers and targeted interventions for early-stage diabetes. Full article

Background: Oxidative stress plays a significant role in inflammatory bowel disease (IBD), yet the clinical relevance of specific lipid peroxidation markers remains insufficiently defined. This study evaluated serum levels of 8-epi-prostaglandin F2α (8-epi-PGF2α), an isoprostane generated through non-enzymatic lipid oxidation, and examined its relationship with antioxidant enzymes and clinical disease activity in ulcerative colitis (UC) and Crohn’s disease (CD). Methods: Eighty-seven patients (55 UC and 32 CD) were assessed for serum 8-epi-PGF2α, superoxide dismutase 1 (SOD1), and glutathione peroxidase 1 (GPX1), and classified as having mild, moderate, or severe disease. Statistical analyses included comparative analysis, two-way ANOVA, multiple linear regression, and Ridge logistic regression. To address potential dietary confounding, total energy intake, Mediterranean Diet Score (MDS), and antioxidant supplement use were incorporated into the regression models. Results: Serum levels of 8-epi-PGF2α and GPX1 were significantly higher in UC than in CD (ρ = 0.001 and p = 0.042), and both increased with greater disease severity (p < 0.001 and p = 0.001). In UC, 8-epi-PGF2α positively correlated with high-sensitivity C-reactive protein (hs-CRP), white blood cells (WBC), and Truelove–Witts Index (TWI), and negatively with hemoglobin (False Discovery Rate (FDR)-adjusted q < 0.100). In CD, it correlated with the Harvey–Bradshaw Index (HBI) and disease duration (FDR-adjusted q < 0.050). Inter-biomarker analyses showed a strong association between 8-epi-PGF2α and GPX1 in UC (ρ = 0.677, p < 0.0001, FDR < 0.0001), suggesting coordinated activation of oxidative and antioxidant pathways. The observed associations remained consistent after adjustment for dietary factors, supporting the robustness of the findings. Because these results are cross-sectional, they cannot establish causality and should be interpreted with caution. Conclusions: Nevertheless, 8-epi-PGF2α emerges as a promising non-invasive biomarker for assessing oxidative stress and disease activity in IBD, with potential clinical applicability for patient monitoring and therapeutic evaluation. Full article

Amino acids are essential nutrients for both tumor growth and immune cell function. Cancer cells actively deplete intracellular and extracellular amino acid pools, and limited amino acid availability in the tumor microenvironment (TME) reinforces immunosuppression. Mitochondria are not merely adenosine triphosphate-producing organelles. Amino acid metabolism within mitochondria contributes to tumor progression and influences immune cell fate and effector function. These effects are mediated through biosynthetic precursor generation for lipid, nucleotide, and polyamine synthesis, maintenance redox homeostasis through glutathione and NAD⁺ metabolism, and regulation of gene expression through aryl hydrocarbon receptor signaling. In this review, we discuss four major mitochondrial amino acid metabolic pathways: glutamine-driven anaplerosis, serine/glycine-dependent one-carbon metabolism, arginine–ornithine metabolism, and tryptophan–kynurenine metabolism. We examine how these pathways are rewired in cancer cells, how they influence immune cell function through direct or mitochondria-associated mechanisms, and how such metabolic reprogramming promotes tumor progression while impairing antitumor immunity. Finally, we consider therapeutic strategies to improve cancer immunotherapy by targeting amino acid metabolism, including mitochondrial metabolic enzymes. This review may help guide the development of more effective metabolic biomarkers and mitochondria-based therapeutic strategies for cancer immunotherapy. Full article