Search Results (1,306)

Dysregulated redox signaling, mitochondrial dysfunction and impaired autophagy form an interconnected network that drives inflammatory and immune responses in cardiovascular disease. Among these, disturbances in redox balance, largely mediated by reactive oxygen species (ROS), serve as key drivers linking inflammatory signaling to adverse cardiovascular outcomes. Mitochondria are essential for energy production and cellular homeostasis, but their dysfunction leads to the accumulation of excessive ROS, which triggers inflammation. This pro-oxidative milieu disrupts immune regulation by activating inflammasomes, promoting cytokine secretion, triggering immune cell infiltration and ultimately contributing to cardiovascular injury. Conversely, intracellular degradation processes such as mitophagy alleviate these effects by selectively eliminating dysfunctional mitochondria, thereby decreasing ROS levels and maintaining immune homoeostasis. These interconnected processes influence myeloid cell function, including mitochondrial reprogramming, macrophage polarization and autophagic activity. The modulation of these immune responses is crucial for determining the severity and resolution of cardiac and vascular inflammation, and consequently the extent of cellular injury. This review examines the latest developments and understanding of the intricate relationships between redox signaling, mitochondrial dysfunction, autophagy and oxidative stress in modulating inflammation and immune responses in cardiovascular diseases. Understanding these interrelationships will inform future studies and therapeutic solutions for the prevention and treatment of cardiovascular diseases. Full article

One way to counteract the effects of environmental stresses, including drought, is to use products with growth-promoting properties for plants. Such agents include quercetin, which is known for its antioxidant and photosynthesis-enhancing properties. In the conducted experiment, the influence of the quercetin–copper complex (Q-Cu (II)) treatment, characterized by strong high solubility in water and strong antioxidant properties, was investigated. The pot experiment demonstrated the effect of spraying with Q-Cu (II) solutions (0.01, 0.05 and 0.1%) on wheat plants growing under drought stress conditions. Two treatments of Q-Cu (II) solutions were applied, and chlorophyll content and chlorophyll fluorescence (the maximum quantum yield of photosystem II (PSII) photochemistry (F_v/F_m), the efficiency of the water-splitting complex on the donor side of PSII (F_v/F_o), and the photosynthetic efficiency index (PI)), as well as gas exchange (photosynthetic network intensity (P_N), transpiration rate (E), stomatal conductance (g_s) and intercellular CO₂ concentration (C_i)), were measured 1 and 7 days after each treatment. In addition, antioxidant enzyme activity (catalase (CAT), peroxidase (SOD) and guaiacol peroxidase (GPOX)) and reactive oxygen species (ROS) levels were determined. Drought stress caused a decrease in chlorophyll content, and values of parameters F_v/F_m, F_v/F_o, PI and P_N, E, g_s, C_i, as well as an increase in ROS levels and antioxidant enzyme activity. Exogenous Q-Cu (II) improved photosynthetic indices and modulated redox status in a dose-dependent manner: 0.01–0.05% reduced ROS, whereas 0.1% increased ROS while concomitantly enhancing antioxidant enzyme activities and photosynthetic performance, consistent with ROS-mediated priming. The conducted research indicates the possibility of using Q-Cu (II) as a product to enhance the efficiency of the photosynthetic process under drought stress. Full article

Ischemia–reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) and a major driver of progression to chronic kidney disease (CKD). Oxidative stress is recognized as a central mediator of this transition. Engulfment and Cell Motility 1 (ELMO1) regulates cytoskeletal remodeling and reactive oxygen species generation through Rac1 activation, but its contribution to CKD progression remains poorly defined. To investigate this, we established a unilateral renal IRI model in wild-type (WT) and Elmo1-overexpressing (Elmo1^H/H) mice and evaluated kidney function one and four months post-IRI. Compared with WT, Elmo1^H/H mice developed more severe kidney dysfunction, including an elevated plasma cystatin C and urinary albumin-to-creatinine ratio, reduced estimated glomerular filtration rate (eGFR), and pronounced fibrosis and glomerular injury observed by light and electron microscopy. Molecular analysis confirmed the dysregulation of redox-related pathways by RT-qPCR, with RNA sequencing showing enrichment of oxidative stress signatures. A subset of mice received chronic vitamin B12 (B12) supplementation following IRI to evaluate its therapeutic potential. Vitamin B12 supplementation improved kidney function, reduced fibrosis, preserved glomerular structure, and normalized the expression of antioxidant genes in both groups. These findings identify Elmo1 as a driver of redox-mediated kidney injury and support vitamin B12 as a promising antioxidant therapy for AKI-to-CKD progression. Full article

Mancozeb is a broad-spectrum fungicide used extensively in agriculture to protect crops against a wide range of plant diseases. Although its capacity to induce oxidative stress is well documented, the cytotoxic effects of mancozeb on red blood cells (RBCs) remain poorly characterized. The present study aimed to investigate the cytotoxic effects of mancozeb on isolated RBCs, with particular focus on oxidative stress-induced cellular and molecular alterations. Human RBCs were exposed to mancozeb (0.5–100 µM) for 24 h. No hemolytic activity was observed across the tested concentrations. However, 10 and 100 µM mancozeb induced a significant increase in intracellular reactive oxygen species (ROS), leading to lipid and protein oxidation and impaired Na⁺/K⁺-ATPase and anion exchanger 1 (AE1) function. These changes resulted in altered RBC morphology, reduced deformability, and increased methemoglobin levels. Alterations in glycophorin A distribution, anion exchanger 1 (AE1) clustering and phosphorylation, and α/β-spectrin and band 4.1 re-arrangement indicated disrupted membrane–cytoskeleton interactions. A release of extracellular vesicles (EVs) positive for glycophorin A and annexin-V was also observed, consistent with plasma membrane remodeling. Despite increased intracellular calcium, eryptosis remained minimal, possibly due to activation of protective estrogen receptor (ER)-mediated pathways involving ERK1/2 and AKT signaling. Activation of the cellular antioxidant system and the glutathione redox system (GSH/GSSG) occurred, with catalase (CAT) playing a predominant role, while superoxide dismutase (SOD) activity remained largely unchanged. These findings offer mechanistic insights regarding the potential health impact of oxidative stress induced by pesticide exposure. Full article

Bacterial outer-membrane vesicles (OMVs) mediate stress tolerance, biofilm formation, and interkingdom communication, but their role in beneficial endophytes remains underexplored. We isolated 11 non-redundant isolates associated with Bacillus, Enterococcus, Kosakonia and Kocuria from Agave tequilana seeds, identified by MALDI-TOF MS and 16S rRNA gene sequencing. We focused on the catalase-negative Enterobacter cloacae SEA01, which exhibits plant-promoting traits and support agave growth under nutrient-poor microcosms. In addition, this endophyte produces OMVs. Time-resolved SEM documented OMV release and cell aggregation within 9 h, followed by mature biofilms at 24 h with continued vesiculation. Purified OMVs (≈80–300 nm) contained extracellular DNA and were characterized by dynamic light scattering and UHPLC–ESI–QTOF-MS lipidomics. The OMV lipidome was dominated by phosphatidylethanolamine (~80%) and was enriched in monounsaturated fatty acids (16:1, 18:1), while the stress-associated cyclopropane fatty acids (17:1, 19:1) were comparatively retained in the whole-cell membranes; OMVs also exhibited reduced ubiquinone-8. SEA01 is catalase-negative, uncommon among plant-associated Enterobacter, suggesting a testable model in which oxidative factors modulate OMV output and biofilm assembly. These may have implications for recognition and redox signaling at the root interface. Future works should combine targeted proteomics/genomics with genetic or chemical disruption of catalase/OMV pathways. Full article

Introduction: Sarcopenia, the progressive age-related decline in skeletal muscle mass, strength, and function, represents a major contributor to morbidity, frailty, and reduced quality of life in older adults. Oxidative stress and chronic low-grade inflammation are increasingly recognized as central mechanisms driving its onset and progression, through pathways involving mitochondrial dysfunction, impaired satellite cell activity, and dysregulated protein turnover. Objective: The purpose of the following manuscript is to summarize current research on the molecular and cellular interactions between oxidative stress and inflammation in sarcopenia, as well as to assess Aronia melanocarpa’s potential as a nutritional intervention. Methods: A narrative review was conducted by searching PubMed, Scopus, and Web of Science for peer-reviewed literature published between 2000 and 2024. Keywords included “sarcopenia”, “oxidative stress”, “inflammation”, “Aronia melanocarpa”, “polyphenols”, and even “functional foods”. Eligible publications provided mechanistic, preclinical, or clinical findings on skeletal muscle biology and A. melanocarpa bioactivity. Results: This narrative review examines the relationship between oxidative stress and inflammation in sarcopenia, focusing on NF-κB-mediated inflammatory signaling, Nrf-2-dependent antioxidant defenses, myokines like myostatin and irisin, and macrophage polarization in muscle homeostasis. Aronia melanocarpa (black chokeberry) is highlighted as a polyphenol-rich fruit with a distinct profile of anthocyanins and proanthocyanidins that have strong antioxidant and anti-inflammatory properties. According to preclinical, clinical, and nutritional studies, A. melanocarpa bioactives modulate redox balance, suppress pro-inflammatory cytokine production, increase antioxidant enzyme activity, and regulate metabolic and regenerative signaling pathways important for skeletal muscle health. Conclusions: Overall, the data suggest A. melanocarpa’s potential as a functional food and nutraceutical candidate for the prevention and treatment of sarcopenia. However, further translational and clinical research is needed to determine the appropriate intake, bioavailability, and long-term efficacy in human populations. Full article

Pinus massoniana, a critically important afforestation species in subtropical China, shows severe adventitious rooting recalcitrance linked to endogenous gibberellin (GA) dysregulation. Our study reveals a GA₄-mediated regulatory network that coordinates hormonal crosstalk, redox homeostasis, and cell wall remodeling. Treatment with the GA biosynthesis inhibitor paclobutrazol (PBZ, 100 mg·L⁻¹) shortened rooting time by 32.5% and increased rooting success by 79.5%. We found that PBZ redirected GA flux by upregulating GA₃-oxidase (GA₃OX), leading to GA₄ accumulation. However, elevated GA₄ levels impaired root development by triggering suberization through ferulic acid (FA)-mediated redox imbalance. Application of GA₄ (100 mg·L⁻¹) reduced caffeoyl alcohol content by 54.4% but increased FA and caffeic acid levels 2.4–3.9-fold, shifting lignin precursors toward suberin biosynthesis. FA modulated H₂O₂ flux in a dose-dependent manner: 200 mg·L⁻¹ optimized redox homeostasis (93.7% lower H₂O₂ influx), whereas 1000 mg·L⁻¹ suppressed mitosis. The combination of PBZ (100 mg·L⁻¹) and FA (200 mg·L⁻¹) synergistically enhanced rooting success by 34.4% and achieved 95.8% field survival after two years (vs. 68.5% in controls), challenging the traditional view that lignification alone limits rooting in woody plants. This work provides the first evidence that the GA₄-FA axis controls adventitious root formation in conifers via a Reactive oxygen species (ROS)-dependent switch between suberin and lignin metabolism, offering new strategies to overcome rooting barriers. The PBZ + FA protocol enables scalable clonal propagation of recalcitrant conifers, with potential applications in molecular breeding and forest restoration. Full article

Hypoxia, oxidative stress, and impaired protein folding contribute to tumor progression and therapy resistance. Endoplasmic Reticulum Oxidoreductin 1 Alpha (ERO1α) is a key enzyme regulating redox homeostasis in the endoplasmic reticulum by reoxidizing protein disulfide isomerase, facilitating disulfide bond formation, and generating reactive oxygen species. Elevated ERO1α levels are associated with increased tumor aggressiveness, metastasis, and poor clinical outcomes. Despite growing evidence of its tumor-promoting functions, no clinically approved ERO1α inhibitors exist. This systematic review provides a comprehensive and integrative analysis of current research on ERO1α in breast cancer, emphasizing its roles in hypoxia response, angiogenesis, immune modulation, and ferroptosis resistance. We discuss mechanistic links, including VEGF-A maturation and PD-L1-mediated immune evasion, and highlight recent advances in small-molecule ERO1α inhibitors and preclinical therapeutic strategies. By consolidating molecular insights and translational considerations, this review underscores ERO1α as both a promising therapeutic target and potential prognostic marker, offering guidance for future drug development and targeted interventions in redox-dependent cancer pathways. Full article

Autophagy and oxidative stress influence cardiovascular pathology. Autophagy mediates lysosome-dependent clearance of damaged proteins and organelles and maintains mitochondrial quality control, proteostasis, and metabolic flexibility. Reactive oxygen species (ROS) originate from mitochondrial respiration and enzymatic reactions during stress. At physiological levels, ROS function as redox signals that activate degradation and recycling, whereas excess oxidants damage lipids, proteins, and nucleic acids and promote cell loss. This review integrates evidence across cardiovascular disease, including atherosclerosis, ischemia reperfusion injury, pressure overload remodeling, heart failure, diabetic cardiomyopathy, arrhythmia, aging, and inflammation. Full article

High-risk human papillomaviruses (HPVs), particularly types 16 and 18, drive carcinogenesis by rewiring host metabolism and mitochondrial function. The oncoproteins E5, E6, and E7 collectively induce mitochondrial fragmentation, increase reactive oxygen species (ROS), and promote a metabolic shift from oxidative phosphorylation (OXPHOS) to glycolysis (the Warburg effect). A redox-sensitive mitochondrial protein, Reactive Oxygen Species Modulator 1 (ROMO1), has emerged as a key mediator of these processes. ROMO1 contributes to mitochondrial morphology, regulates ROS homeostasis, and interacts with key stress-response pathways. While ROMO1 is overexpressed in many cancers and correlates with poor prognosis, recent data suggest that HPV-associated cervical lesions exhibit a unique biphasic expression pattern, with high ROMO1 levels in early stages and reduced expression in advanced tumors. The underlying molecular mechanisms remain unclear, but may involve HPV genome integration, NF-κB suppression, or epigenetic silencing. Key mechanisms such as how HPV modulates ROMO1 expression and how this contributes to stage-dependent metabolic vulnerability remain incompletely understood. This review highlights the current understanding of how HPV oncoproteins impact mitochondrial structure and function, emphasizes the role of ROMO1 in this context, and compares findings with other cancer types. Although no ROMO1-targeted therapies currently exist, the protein may serve as a redox-sensitive biomarker and potential vulnerability in HPV-driven tumors. We propose that targeting mitochondrial fragmentation, ROS signaling, or metabolic reprogramming may offer new avenues for therapeutic intervention. Further research is needed to clarify ROMO1’s dual role in early vs. late-stage disease and to validate its relevance as a clinical target. Our review fills a gap in the current literature by being the first to systematically explore ROMO1’s contribution to HPV-induced mitochondrial dysfunction and metabolic rewiring, and we outline research priorities for future studies. Full article

Age-related macular degeneration (AMD) is a leading cause of irreversible visual impairment in the elderly, and oxidative stress, primarily mediated by reactive oxygen species (ROS), is widely recognized as a central driver of its onset and progression. The retina is highly susceptible to oxidative damage due to its elevated oxygen consumption, abundant polyunsaturated fatty acids, and continuous exposure to light. Recent studies have elucidated molecular mechanisms in which mitochondrial dysfunction, disruption of redox homeostasis, inflammation, and complement activation interact to promote degeneration of retinal pigment epithelium (RPE) and photoreceptor cells. In addition to age-related oxidative stress, environmental factors such as motor vehicle exhaust and volatile organic compounds (VOCs) can accelerate the accumulation of lipofuscin and drusen, thereby fostering a chronic pro-inflammatory milieu. From a therapeutic perspective, beyond conventional antioxidant supplementation, emerging strategies targeting oxidative stress-related pathways have gained attention, including mitochondrial protectants, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, anti-inflammatory agents, and gene therapy. Importantly, several innovative approaches are under investigation, such as saffron supplementation with neuroprotective properties, drug repositioning of levodopa, and nanotechnology-based delivery systems to enhance retinal bioavailability of antioxidants and gene therapies. This review summarizes the pathophysiological role of oxidative stress in AMD from a molecular mechanistic perspective and discusses recent advances in research and novel therapeutic targets. Full article

Anthocyanins, key flavonoid-derived secondary metabolites, not only confer diverse pigmentation but also function in photoprotection, antioxidative defense, and cold acclimation. In woody species, bark anthocyanin turnover is tightly linked to environmental adaptation, stress resilience, and ornamental traits, yet its molecular regulation remains largely unresolved. Here, we investigated Salix alba L. bark by integrating anthocyanin quantification, transcriptome profiling, and weighted gene co-expression network analysis (WGCNA) to dissect the temporal dynamics and regulatory architecture of anthocyanin degradation. Anthocyanin content peaked at D2 (late December 2024), declined through D3 (mid-January 2025) and D4 (mid-February 2025), and partially rebounded at D5 (early March 2025), coinciding with peak expression of structural genes LAC1/2, POD1/2, and BGLU10. These enzymes co-expressed with multiple transcription factors, including MYB, bHLH, and WRKY families, forming putative core modules. Functional enrichment indicated that differentially expressed genes were enriched in redox processes, glycoside hydrolysis, flavonoid metabolism, and hormone signaling, suggesting a degradation mechanism mediated by reactive oxygen species, glycosidic cleavage, and hormone–transcription factor interplay. This study provides the first comprehensive framework of bark anthocyanin degradation in white willow, advancing the understanding of pigment dynamics, gene–environment crosstalk, and breeding strategies for ornamental woody plants. Full article

Background: Recent technological advances have sparked growing interest in high-power laser devices due to their capacity for energy delivery and therapeutic potential, especially in deeper tissues. This promising approach may be comparable to photobiomodulation for modulating inflammatory and redox processes in various tissues. However, to our knowledge, this is the first study to evaluate the safety profile and redox modulation capacity of high-power laser therapy in BV-2 microglial cells. Methods: This study investigated the cellular responses of BV-2 microglial cells exposed to three laser irradiation protocols using a high-power laser device (650/810/915/980 nm, 657 J total dose), applied at variable distances to simulate in vivo power attenuation. Cell viability, apoptosis, adenosine triphosphate(ATP) levels, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), nitric oxide (NO), and intracellular calcium levels were assessed at multiple time points (5 min to 24 h). Results: Protocol-dependent effects were observed. Protocol A promoted early increases in cell viability and ATP levels, along with decreased apoptotic markers and ROS production, suggesting a protective bioenergetic response. In contrast, Protocol C showed transient increases in oxidative stress and reduced MMP, suggesting possible mitochondrial stress. A selective increase in NO levels under Protocol A also suggests modulation of inflammatory pathways without cytotoxicity. Conclusions: High-power laser therapy modulates redox balance, mitochondrial function, and inflammatory mediators (e.g., NO) in a dual-phase manner in BV-2 microglial cells. These findings contribute to defining safe and effective parameters for potential musculoskeletal and neurological applications. Full article

Oxidative stress induces reactive oxygen species (ROS) accumulation, which compromises sperm DNA integrity, cellular homeostasis, and semen quality in Hainan black goats. This study aimed to mitigate ROS-mediated sperm damage by examining the protective effects of curcumin on metabolic regulation and sperm structural integrity. Semen samples were treated in vitro with varying concentrations of curcumin (5, 25, 50 μmol/L) under oxidative stress conditions. The intermediate concentration (25 μmol/L) was most effective at enhancing sperm quality. Following treatment, sperm motility, membrane integrity, and acrosome stability were significantly improved (p < 0.05), while ROS levels and apoptosis rates decreased. Antioxidant enzyme activities—glutathione peroxidase (GPX, p < 0.05), catalase (CAT, p < 0.05), and superoxide dismutase (SOD, p < 0.05)—were markedly elevated. Metabolomic analysis identified 48 differential metabolites (p < 0.05), including gluconic acid, 3-hydroxybutyric acid, and argininosuccinic acid, which were mainly involved in antioxidant defense, energy metabolism (e.g., the citrate cycle), and osmoregulatory pathways. Lipidomics revealed reduced lipid peroxidation and increased polyunsaturated fatty acid content, correlating with enhanced membrane stability. Transmission and scanning electron microscopy revealed preservation of sperm ultrastructure, with reduced mitochondrial and chromatin damage. Quantitative PCR further indicated curcumin-mediated downregulation of pro-apoptotic genes (BAX, Caspase3, and FAS) and upregulation of the anti-apoptotic gene BCL2 (p < 0.05). These findings demonstrate that Curcumin at 25 μM mitigated menadione-induced oxidative stress in goat sperm in vitro, improving antioxidant status, mitochondrial function and membrane integrity while reducing apoptosis. Multi-omic profiling supported redox and lipid homeostasis restoration. These findings establish proof-of-principle in an acute oxidative model. Full article

Sulfur metabolism plays an important role in plant growth and environmental adaptation. Sulfate transporters (SULTRs) are essential players that mediate sulfur acquisition and distribution in many plants, thereby influencing the cellular redox homeostasis under abiotic stress. In this study, we identified 16 putative HvSULTRs genes in barley at the genome-wide level. The conservation and divergence of the SULTR gene family were assessed through a phylogenetic tree and gene structure analysis, revealing that these genes are closely distributed along the chromosomes. Furthermore, the expression pattern of SULTRs in multiple tissues, including flower, root, leaf, stem, seeds, female, male, root meristem, and apical meristem, were analyzed among ten land plants using a public database. Interestingly, the expression of HvSULTR2, HvSULTR4, and HvSULTR5 was upregulated after four days of heat treatment, suggesting their importance in barley’s adaptive response to heat stress. In addition, HvSULTR11 was confirmed to be localized at the plasma membrane and display functional interactions with Hv14-3-3A/Hv14-3-3D. In addition, haplotypes of the HvSULTR11 based on SNP (Single Nucleotide Polymorphism) were divided into ten types across 123 barley varieties. Together, these results provide a new clue to clarify the molecular mechanism of SULTRs in stress response and a new candidate gene resource to enhance the stress (e.g., heat and drought) tolerance in barley. Full article