Search Results (13,561)

Inflammation plays a crucial role in defending the body against harmful stimuli and maintaining physiological balance; however, when it becomes chronic, it contributes to the pathogenesis of several long-term diseases, including autoimmune conditions, cardiovascular and neurodegenerative disorders, and various cancers. Although conventional anti-inflammatory drugs provide symptomatic relief, their long-term use is often associated with adverse side effects. This limitation has shifted scientific attention toward naturally occurring bioactive molecules with potent, safer anti-inflammatory activity. Dietary incorporation of phytopharmaceuticals, such as flavonoids, polyphenols, alkaloids, terpenoids, and fatty acids, has been shown to regulate immune and oxidative mechanisms and to modulate key inflammatory signaling cascades, including the NF-κB, mitogen-activated protein kinase (MAPK), and JAK/STAT pathways. These agents also influence cytokine secretion, NLRP3 inflammasome activation, and antioxidant defense mechanisms involving the Nrf2/HO-1 axis. The current review emphasizes the relevance of major natural plant products in therapy, like quercetin and rutin, resveratrol, glycyrrhizin, lycopene, and indole-3-carbinol. Moreover, recent progress in anti-inflammatory research has focused on novel resolution-based strategies that extend beyond inflammation and oxidative stress suppression. In addition, the review discusses innovations including nanoformulation-assisted targeted delivery, specialized pro-resolving lipid mediators such as resolvins and protectins, and microbiota-oriented therapeutic approaches. Additionally, the review highlights the integration of personalized medicine supported by multi-omics technologies to enhance treatment precision and clinical outcomes. By synthesizing findings from preclinical studies and clinical investigations, this work emphasizes the synergistic therapeutic potential of bioactive compounds from natural sources and resolution-enhancing techniques in restoring immune homeostasis and effectively mitigating chronic inflammation. Full article

Background: Intrauterine adhesions, a leading cause of female infertility, frequently recur in 30–62.5% of patients despite hysteroscopic adhesiolysis and adjuvant therapies. Current intrauterine barriers, including injectable hydrogels, often lack sufficient bioactivity and tissue retention, failing to address the underlying pathological inflammation and oxidative stress driving abnormal fibrosis. Methods: Herein, we tailored a reactive oxygen species (ROS)-responsive, mussel-inspired adhesive injectable hydrogel (OHA-CP@TA) to intelligently modulate the inflammatory niche and promote normal endometrial regeneration. OHA-CP@TA was fabricated through Schiff base bonds between oxidized hyaluronic acid (OHA) and phenylboronic acid-modified carboxymethyl chitosan (CMCS-PBA), and boronate ester bonds between CMCS-PBA and tannic acid (TA). Results: OHA-CP@TA exhibited good mechanical strength, injectability, self-healing, and shear-thinning properties, and importantly, robust and stable adhesion to uterine tissue, overcoming endometrial mucus clearance. It also showed favorable in vivo uterine cavity retention for at least 7 days that covered the critical endometrial repair period. Within the postoperative inflammatory milieu, OHA-CP@TA intelligently released TA in a ROS-dependent manner, which effectively scavenged various ROS and significantly alleviated inflammation, and promoted M1 macrophage polarization into M2 phenotype. This targeted ROS scavenging and immunoregulation inhibited endometrium fibrosis progression, evidenced by downregulation of α-SMA and Col-1, and actively promoted endometrial repair and regeneration, demonstrated by enhanced angiogenesis, increased endometrial thickness, and restoration of glandular numbers. Furthermore, OHA-CP@TA exhibited good biocompatibility, in vivo biodegradability and safety. Conclusions: Therefore, OHA-CP@TA represents a promising, clinically translatable strategy for overcoming the limitations of current IUA management. Full article

Background/Objectives: Arsenic (ARS) exposure is a major cause of kidney injury, driven by oxidative stress, inflammation, fibrosis, and apoptosis. This study evaluated the renoprotective effects of morin (MOR) and morin-loaded PLGA nanoparticles (MOR–PGNPs) against ARS-induced nephrotoxicity in rats. Methods: Sixty male Sprague Dawley rats were randomly allocated into six groups (n = 10 per group). The control group received corn oil. The MOR group received MOR (100 mg/kg), and the MOR–PGNPs group received the same dose of MOR encapsulated in PLGA nanoparticles. ARS was administered at 10 mg/kg for 14 days. Co-treated groups received ARS together with either MOR or MOR–PGNPs, with a 28 min interval between administrations. Renal function markers (serum urea, creatinine, uric acid, renal KIM-1), oxidative stress and antioxidant parameters (Nrf2/HO-1, CAT, SOD, GPx, ROS, MDA), inflammatory mediators (TLR4/NF-κB, TNF-α, IL-6, IL-1β), fibrotic markers (TGF-β1, fibronectin), and apoptotic proteins (caspase-3, caspase-8, Bax, Bcl-2) were assessed, alongside histopathological and ultrastructural evaluations. Results: ARS exposure significantly impaired renal function, increased KIM-1, suppressed Nrf2/HO-1 signaling, reduced antioxidant enzyme activities, and elevated ROS and MDA levels. It also activated TLR4/NF-κB signaling, upregulated pro-inflammatory cytokines and fibrotic markers, and increased pro-apoptotic proteins while downregulating Bcl-2. MOR co-treatment partially ameliorated these alterations. MOR–PGNPs produced potentially enhanced protection, restoring kidney function markers, enhancing antioxidant defenses, and markedly attenuating inflammation, fibrosis, and apoptosis. Histopathological and ultrastructural analyses confirmed preservation of glomerular and tubular architecture, mitochondrial integrity, and minimal cytoplasmic vacuolization in the MOR–PGNPs group. Conclusions: MOR–PGNPs at 100 mg/kg effectively mitigated ARS-induced renal damage through antioxidant, anti-inflammatory, antifibrotic, and anti-apoptotic mechanisms, supporting PLGA-based morin nanoparticles as a promising and safe renoprotective strategy. Full article

Cu and Cd, as common heavy metals occurring in the oceans, can induce oxidative stress and toxic responses in marine organisms. Important economic cephalopods inhabit the eastern coastal areas of China, and exposure to Cu and Cd poses a threat to their normal physiological activities, resulting in serious inhibition of their growth. However, the underlying toxicological mechanisms affecting these cephalopods’ larval stages remain to be elucidated. Here, indicators of oxidative stress and transcriptomics were employed to analyze the toxicological mechanisms of S. esculenta larvae exposed to Cd and Cu. GO and KEGG analysis results indicated that material transport, cellular processes, DNA replication, and other processes were inhibited. A comprehensive analysis of a protein–protein interaction network and KEGG pathways was used to explore the mechanism underlying the toxicity of co-exposure to Cu and Cd toward S. esculenta larvae. We found that Cu and Cd induce significant damage and oxidative stress. The results showed that among 20 identified key genes, ITGA4, LAMA1, and LAMC1, which are involved in the adhesion and connection between cells and the extracellular matrix; COL6A1, COL6A3, COL6A4, and COL6A6, which maintain the integrity of the extracellular matrix; and ABCA1, ABCC5, and ABCC7, which regulate the transmembrane transport of Cu and Cd were involved in the mechanism of toxicity. We suggest that co-exposure to the metals primarily inhibits the connection and adhesion between the cells of the larvae and disrupts the structure and function of the extracellular matrix. The results provide a foundation for understanding the toxicological mechanism of S. esculenta and should be of benefit to artificial breeding programs. Full article

Background/Objectives: Sunflower (Helianthus annuus L.) is one of the four major oil crops worldwide and possesses strong stress tolerance. However, salt stress remains limiting in the improvement of sunflower yield and quality. Methods: In this study, the salt-tolerant cultivar P50 and salt-sensitive cultivar P29 were used as experimental materials to conduct transcriptome sequencing on root and leaf samples treated with NaCl. Subsequently, the molecular mechanisms underlying salt tolerance in sunflower were revealed through assembly and splicing, functional annotation, differential expression analysis, enrichment analysis, and transcription factors (TFs) prediction. Results: Results showed that 54,860,184 and 60,601,572 high-quality clean reads were obtained from the two cultivars, respectively. A total of 110,751 all-unigenes were generated after assembly and clustering, of which 77,536 were functionally annotated. A total of 21,332 differentially expressed genes (DEGs) were identified, including 10,306 upregulated and 11,026 downregulated genes. Quantitative real-time PCR validation of 15 DEGs showed a 93.33% consistency rate with the sequencing data. GO enrichment analysis indicated that DEGs were significantly enriched in pathways related to antioxidant enzyme activities. KEGG enrichment analysis demonstrated that DEGs were primarily involved in 15 carbohydrate metabolism pathways, especially starch and sucrose metabolism. In addition, 67 differentially expressed TF families containing 528 DEGs were identified, including bHLH, AP2/ERF-ERF, MYB, C3H, WRKY, EREBP, B3-ARF, and NAC. Conclusions: Our study constructed a comprehensive transcription map of the sunflower response to salt stress and systematically elucidated the molecular mechanisms underlying salt tolerance. The salt-tolerant sunflower cultivar P50 exhibits an efficient salt stress defense system via three core strategies: (i) activating the antioxidant system to rapidly scavenge excess reactive oxygen species and mitigate oxidative damage; (ii) regulating carbohydrate metabolism through starch and sucrose redistribution to provide energy and osmotic protection against physiological drought; and (iii) mobilizing multiple TF families to establish a complex regulatory network for the precise control of downstream functional genes. Full article

Bombyx batryticatus is a traditional Chinese medicinal material derived from Bombyx mori infected by Beauveria bassiana; however, its formation mechanism remains poorly understood. This study compared infection processes in silkworms by two B. bassiana strains with markedly different virulence (highly virulent ZY027 and ARSEF2860). Integrated transcriptomic and proteomic analyses were employed to uncover, for the first time, the molecular basis of B. batryticatus formation at the systems biology level. The results demonstrated significant weight variations in B. batryticatus derived from different fungal strains. ZY027-induced stiff silkworms exhibited higher wet and dry weights than those infected by ARSEF2860. Large-scale gene reprogramming occurred in silkworm hemolymph post-infection, involving marked activation of Toll/Imd immune signaling pathways, ribosome biogenesis, and endoplasmic reticulum stress responses. A notable “uncoupling” between transcriptomic and proteomic profiles was identified, highlighting the critical role of post-translational regulation in host responses. The two strains triggered distinct metabolic reprogramming patterns: ZY027 notably suppressed oxidative phosphorylation and activated detoxification mechanisms, whereas ARSEF2860 presented characteristics of “immune–metabolic optimization.” These findings suggest that B. batryticatus formation involves complex fungus–silkworm molecular interactions in hemolymph, and that fungal strain characteristics are associated with significant differences in host molecular responses and product biomass. The study provides a theoretical foundation and innovative guidance for selecting strains with high B. batryticatus production potential and developing novel entomopathogenic fungal resources. Full article

Interleukin-6 (IL-6) is a cytokine with multiple biological effects. It plays a complex and seemingly paradoxical central role in both the physiological homeostasis and pathological processes of skeletal muscle. Under physiological conditions, particularly during acute exercise, IL-6 produced and secreted by the contracting skeletal muscle itself acts as an important “myokine.” It operates in an autocrine, paracrine, or endocrine manner to regulate systemic energy metabolism, insulin sensitivity, muscle regeneration, and adaptive hypertrophy. This function is crucial for the health benefits conferred by exercise. However, under various pathological conditions—such as cancer cachexia, sepsis, muscular dystrophy, denervation, disuse atrophy, and chronic inflammatory diseases—persistently elevated systemic or local IL-6 levels become a key mediator driving skeletal muscle atrophy, metabolic disorders, and functional decline. This review systematically elaborates on the dual role of IL-6 in skeletal muscle. It provides an in-depth analysis of its downstream signaling pathways (e.g., JAK/STAT, gp130, MAPK, PI3K-Akt) and upstream regulatory mechanisms (e.g., the Piezo1/KLF15 axis, calcium signaling, mitochondrial function, oxidative stress). A particular focus is placed on discussing the distinct biological effects of classical IL-6 signaling versus trans-signaling. Furthermore, we address current challenges in research and practice, including the cell specificity of IL-6 signaling, the complexity of its temporal regulation, the definition of physiological versus pathological concentrations, discrepancies between animal models and human diseases, and the plasticity of its function across different pathological contexts. Finally, this review explores the potential of targeting the IL-6 signaling pathway as a therapeutic strategy for skeletal muscle atrophy and related metabolic diseases. Potential interventions include IL-6/IL-6R monoclonal antibodies, JAK/STAT inhibitors, gp130 modulators, exercise interventions, and nutritional strategies. This aims to provide a theoretical foundation and novel perspectives for future translational research and clinical interventions. Full article

Oxidative stress is a central component of type 1 diabetes (T1D) pathophysiology, contributing to pancreatic β-cell vulnerability and the development of chronic complications. Current therapeutic strategies are primarily focused on glycemic control and do not directly address underlying redox imbalance. Dietary polyphenols, a structurally diverse class of plant-derived compounds, have been investigated for their antioxidant and cytoprotective properties, yet their role in T1D has not been systematically defined. This systematic review evaluates the effects of polyphenols on oxidative stress and glycemic parameters in preclinical models of T1D. Across studies, polyphenols were consistently associated with attenuation of oxidative stress, as evidenced by reductions in lipid peroxidation and reactive oxygen and nitrogen species, along with restoration of endogenous antioxidant defenses, including superoxide dismutase, catalase, and glutathione. These effects were frequently linked to modulation of redox-sensitive signaling pathways, particularly Nrf2-dependent mechanisms. In contrast, glycemic outcomes were heterogeneous and influenced by compound-specific and experimental factors. Modulation of oxidative stress markers was often observed independently of changes in glycemic parameters, suggesting a primary redox-mediated mode of action. These findings provide a mechanistic rationale for prioritizing oxidative-stress-focused endpoints in future translational studies and support the evaluation of polyphenols as adjunctive strategies targeting redox imbalance in T1D. Full article

Background/Objectives: Sleep deprivation (SD) induces the accumulation of reactive oxygen species (ROS) in the intestine, causing inflammation in the intestine, thereby damaging the intestinal epithelial barrier function. As a traditional Chinese medicine, Dendrobium huoshanense (DHS) modulates intestinal flora, maintains the intestinal mucosal barrier, and promotes gastrointestinal motility and digestive secretion. However, the role and mechanism of DHS in improving SD-induced intestinal injury have not been fully studied. Methods: The SD model was established by subjecting rats to complete SD using a specialised SD instrument. Hematoxylin and eosin (HE) staining was performed to evaluate pathological injury in ileal tissues. Enzyme-linked immunosorbent assay (ELISA) and biochemical methods were used to quantify the main inflammatory cytokines, oxidative stress markers, and hypothalamic–pituitary–adrenal (HPA) axis activity. The expression levels of E-cadherin and Occludin proteins in the ileum tissue were analyzed by Western blotting. Additionally, the pH value of ileal mucus, unit secretion, water content, and dry matter weight were measured. Differential metabolites in rat ileum mucus were profiled using ultra-high-performance liquid chromatography–quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). Results: DHS alleviated the pathological injury of the ileum induced by SD. DHS reduced the levels of serotonin (5-HT), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), while increasing interleukin-10 (IL-10) levels, thereby attenuating systemic inflammatory responses. Furthermore, DHS decreased malondialdehyde (MDA) content and elevated glutathione (GSH) and superoxide dismutase (SOD) levels in ileal tissues. DHS also upregulated the protein expression of E-cadherin and Occludin in intestinal tissues. In addition, DHS decreased the pH of ileal mucus, promoted intestinal mucus secretion, and increased dry matter content, facilitating the restoration of the mucus barrier. DHS may alleviate SD-induced ileal injury by modulating steroid hormone biosynthesis. DHS decreased the levels of adrenocorticotropic hormone (ACTH), cortisol (CORT), and corticotropin-releasing hormone (CRH), indicating that DHS suppresses the abnormal activation of the hypothalamic–pituitary–adrenal (HPA) axis. Conclusions: In this study, a comprehensive multi-index evaluation showed that DHS could significantly improve the ileal injury caused by SD in rats. The mechanism involved regulating the balance of serum neurotransmitters and inflammatory factors, reducing oxidative stress in tissues, and improving the physicochemical properties of intestinal mucus. Metabolomic analysis further revealed that these protective effects may be mediated via the regulation of steroid hormone biosynthesis pathways and are associated with the inhibition of abnormal HPA axis activation. Full article

Background/Objectives: Combination strategies involving natural compounds are increasingly being evaluated to improve the efficacy and safety of conventional chemotherapeutic agents. Quercetin (Q), a bioactive flavonoid, has been reported to regulate oxidative stress and apoptosis-associated signaling pathways. This study investigated whether Q enhances doxorubicin (DOX)-mediated cytotoxicity in OVCAR3 ovarian cancer cells, with particular emphasis on apoptosis, oxidative stress, and EGFR/FOXP3 signaling, while also assessing relative toxicity in HaCaT non-tumoral keratinocytes. Methods: Cell viability was determined using the MTT assay, and drug interactions were assessed according to the Combination Index (CI) method. Apoptosis was evaluated by Annexin V/PI flow cytometry. Caspase-3 and caspase-9 activities were measured using colorimetric assays. Intracellular reactive oxygen species (ROS) production was analyzed using the DCFH-DA assay. EGFR and FOXP3 gene expression levels were quantified by qRT-PCR, whereas caspase-9 protein expression was assessed immunocytochemically. Results: The DOX+Q combination produced synergistic cytotoxic effects in OVCAR3 cells (CI < 1). Compared with OVCAR3 cells, HaCaT cells displayed higher IC₅₀ values following DOX treatment (7.03 µM vs. 1.42 µM) and Q treatment (183.92 µM vs. 35.94 µM), indicating relatively lower treatment sensitivity and suggesting a potentially favorable selectivity tendency; however, these findings should be regarded as preliminary. Flow cytometric findings demonstrated markedly increased proportions of both early and late apoptotic cells following combination treatment. Caspase-3 and caspase-9 activities were significantly elevated after combined exposure (p < 0.01). ROS production increased substantially in response to DOX+Q treatment, corresponding to an approximately 6.82-fold elevation relative to the control group. qRT-PCR analysis demonstrated reduced EGFR and FOXP3 mRNA expression levels in the combination-treated group. Immunocytochemical evaluation additionally revealed stronger caspase-9 staining intensity in treated OVCAR3 cells. Conclusions: These findings suggest that Q may potentiate DOX-induced cytotoxicity through mechanisms associated with enhanced oxidative stress, activation of apoptotic pathways, and modulation of proliferative signaling. The comparatively lower sensitivity observed in HaCaT cells may indicate a possible selectivity tendency; however, these observations remain preliminary and require further validation through in vivo and translational studies. Full article

Background/Objectives: Mild traumatic brain injury (mTBI) is common and may result in persistent cognitive and affective disturbances driven, at least in part, by delayed secondary injury mechanisms, including oxidative stress, neuroinflammation, apoptosis-related signaling, and impaired neuroplasticity. Pharmacological strategies targeting these interconnected processes remain limited. The present study investigated leucovorin, also known as folinic acid, a clinically approved reduced folate, as a potential repurposing candidate in an experimental model of mTBI. Methods: Male Wistar rats were subjected to mild diffuse brain injury using a modified weight-drop model and received a single intraperitoneal dose of leucovorin (20 mg/kg). Behavioral performance was evaluated using the open field, elevated plus maze, forced swim, and novel object recognition tests. Oxidative stress markers, including total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI), as well as inflammatory mediators tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2), caspase-3, brain-derived neurotrophic factor (BDNF), and acetylcholinesterase (AChE), were measured in hippocampal tissue and plasma. Histopathological and immunohistochemical evaluations were also performed in cortical and hippocampal regions. Results: Experimental mTBI was associated with anxiety-like and depressive-like behaviors and impaired recognition memory, whereas basal locomotor activity was not significantly altered. Trauma was also associated with increased oxidative stress, elevated inflammatory and apoptosis-related markers, reduced BDNF levels, altered AChE activity, and histopathological abnormalities. Compared with untreated mTBI animals, leucovorin-treated animals showed attenuation of biochemical and tissue alterations, accompanied by improved behavioral outcomes. Immunohistochemical findings were consistent with reduced inflammatory labeling and relative preservation of tissue architecture following leucovorin treatment. Conclusions: Leucovorin attenuated behavioral, biochemical, histopathological, and immunohistochemical alterations associated with experimental mTBI. These findings suggest that leucovorin may have neuroprotective potential in this setting; however, further studies are needed to clarify the underlying mechanisms, optimal treatment paradigms, and translational relevance. Full article

Nitric oxide (NO) and hydrogen sulfide (H₂S) are key gasotransmitters that regulate multiple aspects of plant growth, development, and stress adaptation. Although their individual signaling pathways have been extensively investigated, the integrated mechanisms underlying NO–H₂S crosstalk and its potential agronomic applications remain unclear. This review summarizes current advances in understanding the biochemical interplay between NO and H₂S in plants, emphasizing their synergistic roles in redox regulation, antioxidant activation, ion homeostasis, and photosynthetic protection under abiotic and biotic stresses. Special attention has been given to recent progress in nanotechnology-based delivery systems that enable the controlled, localized, and sustained release of gasotransmitters, thereby improving bioavailability and minimizing environmental losses. Studies on foliar, seed, and nutrient-solution applications have demonstrated that combined NO/H₂S treatments increase stress tolerance by activating the ascorbate–glutathione (AsA–GSH) cycle, reducing the expression of oxidative markers such as hydrogen peroxide (H₂O₂) and malondialdehyde (MDA), and improving both short-term (Fv/Fm, antioxidant enzyme activity) and long-term (biomass, SPAD index, yield) physiological outcomes. By integrating molecular insights with applied strategies, this review outlines the emerging potential of NO–H₂S signaling as a sustainable tool for crop management in the context of climate change and food security. Full article

Migraine is a complex neurovascular disorder with a multifactorial pathophysiology involving genetic, metabolic, and environmental factors. Increasing evidence indicates that oxidative stress plays a key role in the development of migraine; however, it is unclear whether oxidative imbalance acts primarily as a causal factor or occurs as a consequence of migraine-related processes. Oxidative stress, defined as an imbalance between reactive oxygen species production and antioxidant defense mechanisms, contributes to neuronal hyperexcitability, mitochondrial dysfunction, and neuroinflammation—key mechanisms underlying migraine pathogenesis. Studies have shown elevated markers of oxidative damage and altered antioxidant enzyme activity in migraine patients. Simultaneously, metabolic and inflammatory changes associated with migraine may further exacerbate oxidative imbalance, suggesting a bidirectional relationship. Furthermore, genetic factors such as SOD2, GPX1, and CAT significantly influence susceptibility to oxidative stress and migraine. The CALCA gene, encoding CGRP, links oxidative stress mechanisms with neurogenic inflammation and activation of the trigeminovascular system. This article reviews the current evidence regarding the role of oxidative stress in migraine and discusses its relationship to molecular and genetic mechanisms. Particular attention is given to genes involved in oxidative pathways, mitochondrial function, and inflammatory responses, which may help explain individual susceptibility and variability in clinical presentation. 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

Burn injury induces profound immune dysregulation that extends beyond the acute phase of wound healing, contributing to complications such as delayed repair, infection, and long-term immune dysfunction. Importantly, these effects are not restricted to severe trauma, as similar immune alterations occur following small- to moderate-sized burns. Despite increasing recognition of post-burn immune dysregulation, targeted immunomodulatory therapies remain limited. In this review, we synthesize current insights into the mechanisms driving immune dysfunction after burn injury and outline therapeutic strategies aimed at restoring immune homeostasis. We examine approaches targeting inflammatory triggers and mediators, including acute clinical interventions, reduction in microbial burden, and inhibition of immune cell activation through systemic and local delivery. We also explore strategies to modulate dysregulated innate immune responses by targeting cell-specific functions, such as neutrophil activity and monocyte/macrophage polarization. Persistent activation and exhaustion of the adaptive immune system may be alleviated through interventions such as β-adrenergic blockade, while metabolic, endocrine, and oxidative stress pathways represent additional therapeutic targets. Finally, we highlight key challenges, including the need for improved diagnostics, early prognostic stratification, and personalized treatment approaches to improve outcomes following burn injury. Full article