Search Results (404)

Background/Objectives: The kinetics of blood volume and hemoglobin mass (Hbmass) adaptation in newcomers to moderate altitude and the time required to reach the hematological phenotype of long-term residents remain poorly defined. We aimed to characterize this trajectory over six months and to compare newcomers with established altitude residents. Methods: Thirty-seven healthy male sea-level newcomers were prospectively followed at baseline (within 48 h of arrival), two months, and six months after relocation to Abha, Saudi Arabia (2250 m). Hbmass, blood volume (BV), plasma volume (PV), and red blood cell volume (RBCV) were measured by CO rebreathing; lean body mass (LBM) was assessed by DXA. Six-month values were compared with 107 long-term male altitude residents. Linear mixed-effects models with Holm–Bonferroni correction were used. Results: Adaptation followed a biphasic trajectory. At two months, RBCV and Hbmass rose significantly from baseline (RBCV + 186 mL, Hbmass + 65 g; both p ≤ 0.005), confirmed by LBM-adjusted analysis. These gains partially regressed by six months, after which no volume parameter differed significantly from baseline. Hemoglobin (Hb) and hematocrit (Hct) remained persistently elevated (+6 g/L, +1.9%; both p < 0.001) due to sustained PV contraction. Compared with long-term residents, six-month newcomers had significantly lower LBM-adjusted Hbmass (15.7 vs. 18.0 g/kg), RBCV (48.0 vs. 54.2 mL/kg), and BV (98.9 vs. 109.8 mL/kg; all p < 0.001), yet Hb and Hct were not significantly different. Conclusions: Moderate altitude acclimatization follows a transient two-month erythropoietic increase, then partial regression. Six months is insufficient to attain the oxygen-carrying capacity of long-term residents’ deficit entirely masked by Hb and Hct. Direct Hbmass measurement normalized to LBM is required for accurate assessment of altitude adaptation. Full article

Alzheimer’s disease (AD) is a complex neurodegenerative disorder with limited effective therapies. In this study, a series of 2-(arylamino)thiazol-4(5H)-one derivatives was synthesized using an efficient microwave-assisted protocol, and evaluated for neuroprotective effects against 6-hydroxydopamine (6-OHDA)-induced oxidative stress (OS) in SH-SY5Y neuronal cells and an Aβ42-expressing Drosophila melanogaster model of AD. Among the synthesized compounds, 3n, 3i, and 3b exhibited low cytotoxicity and significant neuroprotection, as evidenced by increased cell viability, reduced reactive oxygen species (ROS) production, and preserved mitochondrial membrane potential. Notably, compound 3n demonstrated the highest activity and effectively ameliorated Aβ42-induced behavioral deficits in vivo. Molecular docking studies predicted favorable binding affinity within the acetylcholinesterase (AChE) active site, with the thiazol scaffold and aryl substituents stabilizing ligand binding through π–π stacking and hydrophobic interactions; compound 3n also formed additional hydrogen bonds enhancing its affinity. Consistent with the docking predictions, in vitro AChE inhibition studies demonstrated that compounds 3n, 3i, and 3b inhibited AChE in a concentration-dependent manner. Network pharmacology predicted seven potential core targets implicated in AD pathogenesis and related pathways, including OS, neuroinflammation, and synaptic dysfunction. Furthermore, in silico pharmacokinetic analysis indicated compliance with Lipinski’s and Veber’s rules, supporting favorable drug-like properties. While further experimental validation is essential, these findings highlight 2-(arylamino)thiazol-4(5H)-one derivatives, particularly compound 3n, as promising multifunctional candidates for further preclinical development against AD. Full article

Drought stress is a major abiotic factor that adversely affects plant growth, development, and crop productivity. Lipoxygenases (LOXs) are key enzymes in the jasmonic acid (JA) biosynthetic pathway and play crucial roles in plant responses to environmental stresses. In this study, the ZmLOX2 gene was cloned from maize (Zea mays L.), and was found to encode a chloroplast-localized 13-lipoxygenase (13-LOX) protein. Expression analysis revealed that ZmLOX2 was predominantly expressed in leaves and was strongly induced under osmotic stress conditions. Compared with wild-type plants, transgenic Arabidopsis thaliana overexpressing ZmLOX2 exhibited significantly higher survival rates, enhanced growth performance, and improved root development under water deficit conditions. Physiological and biochemical analyses showed that the overexpression lines displayed higher activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), accompanied by significantly reduced malondialdehyde (MDA) content and reactive oxygen species (ROS) accumulation. Further investigation demonstrated that the expression levels of JA biosynthesis- and signaling-related genes, including ALLENE OXIDE SYNTHASE (AtAOS), 12-OXOPHYTODIENOATE REDUCTASE 3 (AtOPR3), MYC DOMAIN PROTEIN 2 (AtMYC2), and JASMONATE ZIM-DOMAIN 1 (AtJAZ1), were markedly upregulated in the transgenic lines. Protein–protein interaction analysis suggested that ZmLOX2 may interact with ALLENE OXIDE SYNTHASE 1 (AOS1), HYDROPEROXIDE LYASE 1 (HPL1), and ALPHA-DIOXYGENASE 1 (DOX1). Collectively, these results suggest that ZmLOX2 may contribute to plant adaptation to water limitation by regulating responses associated with JA, enhancing antioxidant defense, and maintaining ROS homeostasis. Full article

Cerebral ischemia–reperfusion injury is a key determinant of a poor outcome after stroke. The mitochondrial uncoupling protein 2 (UCP2) has been implicated in cerebral ischemia-reperfusion injury and in the outcome of ischemic stroke, although its role remains controversial. In C57BL/6J and B6.129S4-Ucp2^tm1Lowl/J (UCP2^−/−) mice, we analyzed cognitive function and lifespan. In an MCAO model induced for one hour, infarct volumes, neurological deficits, and gene expression patterns were determined after 24 h. The UCP2 inhibitor genipin was used in an oxygen-glucose deprivation (OGD) model to investigate synaptic transmission in the hippocampus. Compared to controls, UCP2^−/− mice exhibited a reduced lifespan and displayed impaired cognition. However, in 6-month-old UCP2^−/− mice, the infarct volume was reduced, primarily due to a smaller core size, but not in 18-month-old animals. In both strains, ischemia induced upregulation of antioxidant defense genes, including catalase and SOD1. In the ex vivo ODG model, synaptic transmission was depressed, but pretreatment with genipin prevented the tissue from this impairment. Our findings indicate an infarct-reducing effect of UCP2 deficiency, especially in young-adult mice, and, mechanistically, a neuroprotective effect by genipin in hippocampal slices. Full article

Background: Idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF) are defined and monitored without definite exercise-based criterion, despite exertional desaturation being among the earliest functional signs of disease and an established independent predictor of mortality in IPF. The 6 min walk test (6MWT) provides robust prognostic information in IPF, yet whether it can kinetically distinguish IPF from PPF under sustained submaximal loading has not been systematically examined. We hypothesised that second-by-second oximetry during the 6MWT and the 1 min (min) sit-to-stand test (1STST) would expose phenotype-specific kinetic signatures invisible to static endpoints, and that test modality would matter. Methods: Fifty-one patients with IPF, 12 with PPF, and 100 with non-IPF/non-PPF ILD (reference cohort) from the European ILD Registry (eurILDreg) participated in this pilot study and completed both tests with continuous 1 Hz SpO₂ and pulse-rate recording. Phenotype-specific desaturation and recovery slopes were derived from random-effects panel regression models. Multivariable linear regression tested whether IPF and PPF phenotypes carried kinetic and static-endpoint signatures independent of DLCO, age, sex, and BMI. Results: Despite substantially lower DLCO in fibrosing phenotypes (IPF 45 ± 17%, PPF 38 ± 11%, reference 55 ± 19%; p < 0.001), conventional exercise performance metrics did not differ significantly between groups (6MWD p = 0.099; 1STST repetitions p = 0.351). The 6MWT produced statistically indistinguishable per-second desaturation slopes in IPF and PPF (both ≈ −0.016%/s versus −0.011%/s in the reference), whereas the 1STST exposed a clear phenotype gradient (PPF −0.044%/s, IPF −0.027%/s, reference −0.016%/s; a 2.75-fold spread). PPF additionally showed a blunted chronotropic response during the 6MWT (PR slope +0.014 vs. +0.032 and +0.033 bpm/s in IPF and reference). Likelihood-ratio tests confirmed significant phenotype effects on seven of eight time-resolved trajectories (all p < 0.001). IPF was independently associated with greater cumulative oxygenation deficit during the 1STST (SpO₂ AUC β = +669, p = 0.022), indicating excess dynamic burden beyond what diffusion capacity predicts. Conclusions: In this pilot analysis, continuous high-resolution oximetry identified two phenotype-related signals that were robust to the principal confounders. IPF was independently associated with a greater cumulative oxygenation impairment during the 1STST after DLCO adjustment, and PPF showed a blunted chronotropic response during sustained walking that, being pulse-rate based, was unaffected by supplemental oxygen and was not attributable to pulmonary hypertension. A phenotype gradient in per-second desaturation measurements during the 1STST was also observed but should be interpreted as hypothesis-generating, as the small PPF subgroup (n = 12), its greater disease severity, and supplemental oxygen use in half of its patients preclude firm attribution to phenotype. Taken as exploratory, these observations support the prospective evaluation of kinetic exercise parameters as candidate monitoring components for PPF. Full article

Introduction: Survival at high altitudes requires efficient energy management. Although hypobaric hypoxia alters thermodynamic efficiency, the independent impact of altitude versus demographic factors on basal and exertional caloric costs remains uncertain. We evaluated these variables in chronic residents across four Peruvian altitudes. Methodology: A cross-sectional study was conducted involving 141 healthy adults (aged 18–38 years) residing in Lima (154 m), Arequipa (2335 m), Puno (3827 m), and La Rinconada (5100 m). Resting energy expenditure (REE) and physical activity energy expenditure (PAEE) were estimated using continuous photoplethysmography; PAEE was assessed following the 6-min walk test (6MWT). Hemodynamic parameters, oxygen saturation (SpO₂), and hemoglobin (Hb) levels were evaluated. An analysis of covariance (ANCOVA) was employed to adjust metabolic variations for age, sex, and body mass index (BMI). Results: Unadjusted data demonstrated a progressive increase in REE and PAEE proportional to altitude. However, the ANCOVA revealed that the independent effect of the city of residence was no longer statistically significant after adjusting for anthropometric and demographic covariates. Physiologically, the SpO₂ deficit imposed a high metabolic demand (an increase of approximately 1.29 kcal in REE for every 1% drop in SpO₂). Hb concentrations above 18 g/dL were associated with an exponential increase in caloric cost driven by blood hyperviscosity. A positive correlation was identified between Hb levels and energy expenditure (EE), which proved to be statistically stronger in the female cohort. Under extreme hypoxia conditions (5100 m), men exhibited a significantly higher PAEE (50.60 ± 10.17 kcal vs. 40.78 ± 5.21 kcal). Despite the increased biological effort, mechanical performance in the 6MWT remained constant across cities. Conclusions: There is no independent relationship between REE and the altitude of residence. The initial unadjusted relationship between altitude and EE was negated by covariates, particularly body mass index (BMI). The preservation of functional capacity at the expense of the energy economy underscores the profound physiological burden of Andean acclimatization. Full article

COVID-19, influenza, and respiratory syncytial virus are leading causes of severe acute respiratory infection (SARI). As viral dynamics shift post-pandemic, comparing their clinical profiles is essential for optimizing management and vaccination strategies. We conducted a retrospective observational study of adults hospitalized with PCR-confirmed COVID-19, influenza, or RSV over three consecutive seasons (2021–2024). We compared clinical features, comorbidities and outcomes, including mortality, intubation rates and respiratory deterioration. Multivariable analyses were performed where virus was the independent variable and respiratory deterioration, intubation rate and mortality, Charlson Comorbidity Index, smoking status and pneumonia were co-variates. 263 patients were analyzed. Key findings revealed distinct clinical profiles: influenza patients were significantly younger, while COVID-19 was the predominant cause of viral pneumonia. RSV patients presented with the most severe oxygenation deficit upon admission and experienced the highest rate of respiratory deterioration (28%). Logistic regression analyses demonstrated that pneumonia [OR 2.81, 95% Confidence Interval (CI): 1.23–6.43, p = 0.01] and RSV (OR 2.8, 95% CI: 1.16–6.63, p = 0.02) were independently associated with respiratory deterioration. Similarly, pneumonia (OR 4.86, 95%CI: 1.62–17.36, p < 0.01] and RSV (OR 4.67, 95%CI: 1.5–14.34, p < 0.01) were independently associated with high risk of intubation. Among patients hospitalized because of COVID-19, RSV and Influenza, pneumonia and RSV were linked with respiratory deterioration and increased risk of intubation but not with death. Full article

Introduction: Diabetic foot ulcers (DFUs) are a debilitating complication of diabetes, and management by multidisciplinary foot teams has been shown to reduce serious sequelae, such as amputations. There are stark racial and ethnic disparities in morbidity and mortality from DFUs, and multidisciplinary care has been shown to reduce lower extremity amputations, length of hospital stays and readmissions. This is a review of the impact of multidisciplinary care on DFUs, particularly regarding social determinants of health, with an illustrative case. Case Presentation: This is a case of a 32-year-old African American male with Type 1 Diabetes, a history of poor glycemic control, attention deficit hyperactivity disorder, tobacco and marijuana use disorder, and multiple social and structural barriers to care. He presented with bilateral Wagner grade 3 DFUs with osteomyelitis to the emergency department, requiring hospitalization. Upon discharge, he was referred to a multidisciplinary diabetes clinic and received coordinated support from endocrinology, podiatry, vascular surgery, infectious disease, pedorthics, and behavioral health. Comprehensive evaluation, intensive wound care with adjuvant hyperbaric oxygen therapy, offloading, blood glucose management and medical source control of infection were established for his treatment plan. At the three-month follow-up, the patient’s wound beds had significantly improved, and his Hemoglobin A1c declined from 12.6% to 9.3%. The right plantar wound completely epithelialized, and the left foot wound showed 90% contracture. Review and Discussion: This case highlights the importance of integrated, multidisciplinary care for DFUs, particularly in addressing both the clinical and social drivers of complications from diabetes. Full article

Alkaline water electrolysis (ALK) is essential for renewable energy integration, yet traditional models using a fixed minimum operating power often overestimate low-load flexibility by neglecting state-dependent safety boundaries. This study develops an electro-thermal-mass multiphysics dynamic model that treats the transient hydrogen content in oxygen (H₂-in-O₂) concentration as a first-principles state variable. Based on a quasi-steady-state safety balance, a dynamic minimum operating power constraint is derived to replace empirical static limits. A key feature of this model is the explicit coupling of Arrhenius thermal diffusion and pressure-differential-driven permeation during load transients, allowing the safety threshold to respond to real-time system states. Year-round simulations of a 30 MW industrial system under a wind–solar time series reveal that thermal inertia, with a time constant of approximately 4.2 h, induces a sustained mismatch between low-power operation and high system temperature. Under high-temperature and rapid-ramp conditions, the dynamic safety lower bound reaches 28.2% of the rated capacity, exceeding the conventional 20% static threshold by 8.2 percentage points. This deviation results in 378.3 MWh of implicit curtailment and 60.5 h of additional downtime annually, leading to a green hydrogen production deficit of approximately 42.2 t/year. This research provides a theoretical foundation and technical reference for the optimal control and flexibility assessment of industrial-scale green hydrogen systems under fluctuating power supply conditions. Full article

Background: Hypoxic–ischaemic brain injury (HI) is a major contributor to neurological deficits following stroke. Understanding what happens to the smallest functional and structural unit of the central nervous system in the face of oxygen and nutrient deprivation is essential to fully comprehend the pathogenesis of diseases and disorders associated with HI, such as ischaemic stroke. Aim: The aim of this study was to develop a robust in vitro tool for initial screening of potential therapeutics and identification of diagnostic markers of brain hypoxic injury. Methods: This study details and validates a comprehensive protocol for modelling HI using differentiated SH-SY5Y neuroblastoma cells (Neuron-like Cells, NLCs). First, we optimized the differentiation process and confirmed the maturity and purity of NLCs via standard molecular markers. The NLCs exhibited functional excitotoxicity, demonstrating a graded cell death response to N-methyl-D-aspartate (NMDA), thus validating their functional application. To simulate HI, we initially optimized the oxygen-glucose deprivation (OGD) treatment using graded concentrations of CoCl₂ (0.125 mM to 2 mM) in glucose-free media. The validated NLCs were then subjected to the refined OGD protocol (1 mM CoCl₂ in glucose-free media) for 3 h, followed by various periods of reoxygenation (1 h, 3 h, 6 h, 12 h, 18 h, and 24 h). Result: Bulk RNA-sequencing revealed a distinct temporal transcriptional response to HI. Injury-associated genes, including heat shock proteins and stress markers, were significantly (p < 0.05) upregulated at 3 h of reoxygenation, peaked at 6 h, and declined thereafter, remaining above baseline at 24 h. Upstream regulator analysis identified IL-1β, TNF-α, and HIF-1α as key drivers during OGD, with additional regulators emerging during reoxygenation. TNF-α and β-oestradiol were consistently identified across time points, while TGF-β1 and NTRK1 became prominent during peak injury and later phases. Analysis of secreted factors showed increased release of inflammatory (TNF-α) and neurotrophic (β-NGF, BDNF, VEGF) mediators with reoxygenation, while maximal cell death occurred at 24 h. Conclusions: This study identifies a transient, time-dependent transcriptional cascade following hypoxic–ischaemic injury, highlighting a critical window for early neuronal response. The model provides a reproducible platform for studying neuronal injury and recovery, and identifies known (TNF-α, IL-β, and HIF-1α), context-specific (NTRK1 and TGF-β) and novel (β-oestradiol) regulators of the injury response with potential relevance for therapeutic targeting. Full article

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) accumulation and a breakdown of mitochondrial homeostasis. Vitamin K2 (VK2) has emerged as a potential neuroprotective agent, yet the specific molecular cascades linking its intervention to the restoration of mitochondrial integrity remain poorly understood. This study utilizes an AD Drosophila model to investigate the efficacy of VK2 and elucidates its multidimensional regulatory mechanisms. Behavioral analysis showed that VK2 significantly rescued locomotor impairments, improving both vertical climbing and horizontal walking performance. Crucially, VK2 intervention achieved a systemic rescue of mitochondrial health: transmission electron microscopy (TEM) confirmed the preservation of mitochondrial ultrastructure and cristae density, while biochemical assays demonstrated a robust recovery of bioenergetic markers, including ATP levels and the NAD⁺/NADH ratio. Furthermore, VK2 treatment stabilized the mitochondrial membrane potential (MMP) and effectively attenuated the accumulation of reactive oxygen species (ROS). To identify the molecular drivers of this recovery, an unbiased integration of human clinical transcriptomic data and network pharmacology prioritized the EGFR-Ras-ERK signaling axis as a central hub. In vivo validation confirmed that VK2 suppresses the pathological overactivation of this cascade. VK2 reduced EGFR phosphorylation in parallel with the effects observed for the EGFR inhibitor Gefitinib. Collectively, our findings show that VK2 ameliorates locomotor deficits and mitochondrial dysfunction in Aβ42-expressing flies and that these effects are associated with suppression of the EGFR-Ras-ERK signaling axis. Further studies are required to establish direct target engagement and pathway causality. Full article

Accurate prediction of contaminant transport and self-purification processes in rivers remains challenging because pollutant dispersion, biochemical reactions, and hydrodynamic conditions interact across multiple spatial scales. This study aims to develop and compare mathematical models for soluble contaminant transport and biodegradable organic matter removal in channels and rivers. Unsteady advection–diffusion–reaction equations were formulated for one-dimensional (1D), two-dimensional (2D), and three-dimensional (3D) transport scenarios and solved through numerical techniques based on the transformation of partial differential equations into systems of ordinary differential or algebraic equations. In parallel, the classical Streeter–Phelps model and an extended formulation incorporating turbulent diffusion were implemented to evaluate organic load degradation and oxygen deficit dynamics. Simulations were performed using a Matlab R2019a-based computational framework under representative hydraulic and reaction conditions obtained from literature data and empirical correlations. The results showed that, under specific conditions, the 3D model reproduced trends comparable to those predicted by the 2D model, while the latter approached the behavior of the 1D formulation. The Streeter–Phelps model predicted an organic load removal efficiency of 97.74%, a purification index of 1.9564, a critical time of 18.43 h, and a critical distance of 6.93 km. These findings provide a useful framework for river water-quality assessment and support future applications involving complex hydrodynamic and pollutant-loading scenarios. Full article

Background/Objectives: Multi-strain Limosilactobacillus fermentum supplementation has been reported to promote weight loss outcomes in free-living conditions, but limited evidence exists on these probiotic strains added to an energy-restricted diet and walking program in overweight adults. Methods: In a double-blind, placebo-controlled, parallel-arm randomized trial, overweight adults (35.2 ± 13.2 years old, 167.6 ± 8.6 cm, 79.9 ± 11.8 kg, 28.4 ± 2.7 kg/m² body mass index, 36.1 ± 6.6% body fat) completed a 12-week weight loss program that included a 500 kcal/day energy deficit and walking 10 k steps/d. Participants ingested one daily capsule containing a three-strain probiotic blend (L. fermentum K7-Lb1, L. fermentum K8-Lb1, L. fermentum K11-Lb3; 6 billion CFU/day) (PRO) or maltodextrin placebo (PLA). Assessments were performed at baseline, week 6, and week 12 and included body composition, resting energy expenditure, substrate utilization, peak oxygen uptake, dietary intake, step counts, blood biomarkers, quality of life, and side effects. Data were analyzed using multivariate and univariate repeated-measures general linear models (GLM), with mean changes from baseline presented alongside 95% confidence intervals. Results: All participants significantly reduced body weight, fat mass, body fat percentage, and waist circumference. At 12 weeks, PRO reduced fat mass more than PL (−2680.7 ± 1276.7 g; p = 0.039). In PRO, android and gynoid fat percentage decreased at 6 weeks (p < 0.001; p = 0.008) and 12 weeks (p = 0.004; p < 0.001), respectively. Visceral adipose tissue mass, volume, and area were lower at 6 weeks and trended lower at 12 weeks. In PRO, bone mineral content and bone mineral area decreased at 12 weeks, while bone mineral density paradoxically increased (0.007 ± 0.003 g/cm²; p = 0.024). Conclusions: During a 12-week weight loss program, supplementation of a multi-strain L. fermentum probiotic significantly reduced body fat and central adiposity. Full article

Oxidative stress is a major contributor to neuronal apoptosis and subsequent neurofunctional deficits. This study investigates the dual role of the mitochondrial membrane-anchored protein NIX in PC12 cells, a model for mature neurons. We demonstrate that both overexpression and knockdown of NIX attenuate apoptosis under oxidative stress, albeit through distinct mechanisms. Overexpression of NIX promotes cell survival by activating NIX-mediated mitophagy, which clears damaged mitochondria and intracellular reactive oxygen species (ROS), thereby maintaining redox homeostasis. Conversely, knockdown of NIX reduces apoptosis primarily by diminishing the intrinsic pro-apoptotic function of the protein. Collectively, these findings reveal that NIX expression levels critically gate PC12 cell fate under oxidative stress by differentially activating pro-survival or anti-apoptotic pathways. Full article

We previously demonstrated that fatty acid-binding protein 3 (FABP3) is significantly upregulated in ischemic neurons, and its inhibition mitigates ischemic brain injury in mice and attenuates mitochondrial damage under rotenone-induced oxidative stress. These findings suggest a potential role for FABP3 in mitochondrial dysfunction in ischemic neurons, although the underlying mechanism remains unclear. In this study, we further investigated the role of FABP3 in mitochondrial injury and apoptosis in ischemic neurons. Our findings indicated that FABP3 deficiency significantly decreased infarct volume following middle cerebral artery occlusion/reperfusion (MCAO/R) in mice, improved cognitive and spontaneous activity deficits, and suppressed BAX activation and mitochondrial translocation, caspase-3 activation, and cytochrome c release. In HT22 cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R), FABP3 deficiency increased cell viability, reduced apoptosis, and alleviated the loss of mitochondrial membrane potential. Conversely, FABP3 overexpression further exacerbated mitochondrial dysfunction and apoptosis, effects that were partially reversed by the BAX inhibitor BAI1. Furthermore, FABP3 overexpression promoted abnormal mitochondrial lipid accumulation and increased lipid peroxidation. Both the mitochondria-targeted antioxidant MitoQ and the ferroptosis inhibitor Ferrostatin-1 alleviated FABP3 overexpression-induced mitochondrial damage and apoptotic signaling. Collectively, our findings suggest that FABP3 is an important promoter of cerebral ischemia–reperfusion injury. FABP3 may aggravate ischemic neuronal injury by promoting abnormal mitochondrial lipid accumulation and lipid peroxidation, thereby enhancing BAX-dependent mitochondrial apoptotic signaling. Targeting FABP3 may provide a potential therapeutic strategy for neuroprotection in ischemic stroke. Full article