Search Results (1,561)

Regular exercise mediates inter-tissue communication between skeletal muscle and the immune system through skeletal muscle-derived secretory factors, providing an important molecular basis for the beneficial effects of exercise on chronic inflammation, metabolic dysregulation, and impaired tissue repair. As key effector cells of the innate immune system, macrophages do not simply conform to a dichotomous classification of classically activated M1 macrophages and alternatively activated M2 macrophages; rather, their functional states constitute a dynamic spectrum shaped by exercise load, recovery time window, tissue microenvironment, and disease context. This review focuses on recent advances in exercise-induced skeletal muscle secretory factors involved in macrophage functional remodeling. Representative signals, including interleukin-6 (IL-6), irisin, meteorin-like protein (METRNL), fibroblast growth factor 21 (FGF21), oncostatin M (OSM), decorin, myostatin, chemokines, and extracellular vesicles, are systematically summarized in terms of their exercise responsiveness, evidence for skeletal muscle origin, and evidence supporting macrophage regulation. Based on these dimensions, an evidence-strength grading framework is further proposed. Moreover, this review integrates key signaling axes, including glycoprotein 130 (gp130)/Janus kinase (JAK)/signal transducer and activator of transcription (STAT), signal transducer and activator of transcription 6 (STAT6)/peroxisome proliferator-activated receptor gamma (PPARγ), AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor kappa B (NF-κB), transforming growth factor beta (TGF-β)/Smad, and chemokine receptor pathways, to explain how exercise-induced secretory networks participate in the dynamic regulation of the macrophage functional spectrum through immune cell recruitment, inflammatory clearance, immunometabolic reprogramming, matrix remodeling, and repair-niche formation. Current evidence indicates the translational potential of exercise-induced skeletal muscle secretory factors in skeletal muscle repair, metabolic inflammation, aging-related functional decline, and cancer rehabilitation. However, this field still faces several major challenges, including insufficient tracing of skeletal muscle-derived signals, limited direct causal validation, a lack of human tissue-level evidence, and unclear exercise dose–response relationships. Future studies should combine tissue-specific genetic interventions, receptor blockade, single-cell and spatial omics, metabolic flux analysis, and standardized human exercise interventions to further clarify the mechanistic basis and application boundaries of exercise-induced skeletal muscle–macrophage communication, thereby providing a theoretical foundation for precision exercise prescription and chronic inflammation intervention. Full article

Background/Objectives: Skin aging involves interconnected inflammatory, oxidative, hormonal, extracellular matrix (ECM), and cellular senescence-related mechanisms, supporting the need for multitarget approaches. This study aimed to evaluate the effects of a multicomponent natural product-based injectable formulation developed in Korean medicine practice, Dong-An Pharmacopuncture (DAP), on skin aging-related pathways. Methods: A network pharmacology approach was used to identify the active compounds, predicted molecular targets, and signaling pathways associated with DAP. Sixty-two active compounds from 11 constituent materials were screened, and 70 final targets were identified using STITCH-based prediction, intersection with GeneCards-derived skin aging-related targets, and quality filtering. Results: Herb-compound-target network analysis yielded 225 compound–target interactions across 292 edges. Protein-protein interaction analysis identified a highly connected network with 1,334 edges, and hub analysis converged on 10 core targets: TNF, IL6, ESR1, TP53, AKT1, PPARG, EGFR, PTGS2, CASP3, and PPARA. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses identified four major mechanistic axes: inflammatory and oxidative stress regulation, hormonal skin homeostasis, tissue repair and ECM remodeling, and cellular senescence-related regulation. Because DAP is administered by injection, a Good Laboratory Practice-compliant single-dose subcutaneous toxicity study was additionally conducted in Sprague–Dawley rats, which showed no mortality, abnormal clinical signs, or histopathological findings attributable to DAP at 1.0 mL/head. Conclusions: The findings in this study provide a systems-level framework for the predicted multitarget mechanisms of DAP in skin aging-related pathways and support the need for further experimental validation of its predicted mechanisms and repeated-dose safety. Full article

Gaseous air pollution is a major environmental risk factor for atherosclerosis, yet the specific molecular networks linking Gaseous air pollution to atherosclerosis are not fully characterized. This study aimed to elucidate how gaseous pollutants drive atherosclerosis using a multi-level framework integrating network toxicology, nine machine-learning algorithms, bulk and single-cell/spatial transcriptomics, molecular docking, clinical tissue/serum validation, and in vitro pollutant-exposure assays. A conserved RXRA–MMP9–TNF axis was identified as a core molecular network linking pollutant exposure to atherosclerosis. Single-cell and spatial transcriptomics showed broad expression of RXRA (Retinoid X Receptor Alpha) in vascular stromal and endothelial cells and its association with xenobiotic and lipid metabolism, whereas MMP9 (Matrix Metallopeptidase 9) and TNF (Tumor Necrosis Factor) were enriched in macrophages, T cells, and mast cells within plaques, correlating with immune cell infiltration. Multiple pollutants displayed high binding affinity to these proteins. Clinical samples showed upregulation of these targets in atherosclerotic tissue and serum. Toluene exposure in THP-1-derived macrophages significantly increased RXRA, MMP9, and TNF mRNA and protein levels. These findings highlight an immune–metabolic interplay centered on the RXRA–MMP9–TNF axis in Gaseous air pollution-driven atherosclerosis, supporting these molecules as candidate biomarkers for environmental health strategies. Full article

The SUN family protein MoSun4 in Magnaporthe oryzae has been previously implicated in mitophagy and has potential as a target for reducing rice blast, but its role as a secreted protein remains poorly understood. In this study, signal peptide prediction and yeast secretion assays confirmed MoSun4 signal peptide function, and co-localization revealed the localization of the extra-invasive hyphal membrane (EIHM)-associated apoplastic compartment or matrix, establishing MoSun4 as a secreted protein. In addition, deletion of the MoSUN4 gene reduced the hyphal growth, conidiation and virulence of M. oryzae. We further showed that MoSun4 is involved in regulating the expression of virulence-related genes, including multiple genes involved in cell wall degradation (eglC, eglD), secondary metabolism (gliK), and melanin biosynthesis (SDH1, BUF1, Cmr1, ALB1). Collectively, our study reveals that MoSun4 is a secreted protein that contributes to pathogenicity and is associated with altered expression of virulence-related genes, providing new insights into the functions of SUN family proteins. Full article

Oenocarpus bataua Mart. (Arecaceae) (known as “majo” in Bolivia) is an Amazonian palm fruit with considerable potential for the development of functional foods; however, its rapid postharvest deterioration limits its utilization. This study evaluated the effects of preservation methods and frozen storage on the physicochemical properties of two morphotypes of its fruits (dark-purple and pale-colored). Proximate analysis of pulp and peel fractions revealed a lipid-rich composition, with crude lipid contents close to 49% (dry basis), moderate protein levels (7.1–9.7%), and crude fiber contents around 15%. Dietary fiber characterization showed exceptionally high total dietary fiber (61.6%), predominantly insoluble dietary fiber (56.3%) under short-term frozen storage. Fresh pulp exhibited high antioxidant capacity, as determined by the DPPH assay (2003–2070 µmol TE/g dry matter), while freeze-drying preserved significantly higher antioxidant activity than hot-air drying. Functional properties were strongly affected by storage duration, with water-holding capacity decreasing from (4.43–3.17) g H₂O/g dry matter and swelling capacity from 13.95 to 9.62 mL H₂O/g dry matter after prolonged freezing. FTIR spectroscopy confirmed the presence of characteristic polysaccharide and lignocellulosic structures and indicated structural disruption of the insoluble fiber matrix during long-term storage. These findings support the use of Bolivian majo as a promising source of functional ingredients and provide a basis for developing value-added Amazonian food products and optimizing preservation strategies. Full article

Previous studies have indicated that polyethylene terephthalate (PET) micro/nanoplastics (MNPs) may coexist with antibiotics in environmental and biological matrices; however, their combined behavior in blood remains insufficiently characterized. This study examined PET MNPs prepared from water bottles at 0.5, 2.5, and 7.5 mg/mL together with tetracycline (2–50 µg/mL) in defibrinated horse blood. After 24 h exposure and particle removal, UV–visible absorbance, intrinsic fluorescence, redox indicators, and subsequent Escherichia coli responses were evaluated. The blood biochemical results showed condition-dependent changes in hemoglobin-associated absorbance, tryptophan-dominated fluorescence, reactive oxygen species, reduced glutathione, superoxide dismutase, and lipid peroxidation. When treated blood supernatants were applied to Escherichia coli, tetracycline alone reduced bacterial OD600, whereas selected PET MNP–tetracycline co-exposures partially restored bacterial proliferation and modified oxidative-stress responses. ATR–FTIR analysis of Escherichia coli pellets showed dose-dependent modulation of phosphate-, lipid-, and protein-associated bands, indicating changes in bacterial biochemical fingerprints under specific exposure combinations. Overall, the findings suggest that PET MNPs can modify tetracycline-associated spectral, redox, and bacterial response patterns in a blood matrix. Future studies incorporating adsorption assays, free tetracycline quantification, protein-corona profiling, time-course exposure designs, and antibiotic susceptibility testing would further clarify the mechanistic basis and biological relevance of these matrix-dependent interaction effects. Full article

Background: Osteoarthritis (OA) is a prevalent degenerative joint disease with a complex molecular basis. This study aims to identify key molecules involved in OA pathogenesis, focusing on the role of acetylation-related gene expression. Methods: Public microarray datasets GSE82107 and GSE169077 were integrated to construct a differential expression landscape between OA patients and healthy controls. Acetylation-linked differentially expressed genes (acetylation-DEGs, ARDEGs) were extracted by intersecting DEGs with a curated set of acetyltransferases, deacetylases and acetylation substrates. A protein–protein interaction (PPI) network was built and subjected to LASSO-penalized regression to prioritise hub genes. Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG) and Gene Set Variation Analysis (GSVA) were performed to characterize biological themes. Immune infiltration was quantified with CIBERSORTx and single-sample Gene Set Enrichment Analysis (ssGSEA). Single-cell RNA-seq data (GSE216651) were employed for orthogonal validation. For experimental corroboration, synovial tissue was collected from OA patients undergoing arthroplasty; mRNA and protein levels of hub genes were determined by qRT-PCR, Western blot and immunofluorescence. The destabilisation of the medial meniscus (DMM) mouse model was used for in vivo verification. Results: Twenty-one high-confidence ARDEGs were identified. Analysis of the PPI network yielded ten hub nodes, six of which (EGR1, PFKFB3, HDAC4, MMP13, PDK4 and ACADL) retained non-zero coefficients in the least absolute shrinkage and selection operator (LASSO) model. Enrichment analyses implicated these genes in embryonic development, collagen-containing extracellular matrix remodeling and PI3K–Akt signaling. Immune infiltration analysis showed potential differences in immune cell abundance between OA and healthy controls. Single-cell dataset analysis verified the expression patterns of key genes in different cell types. Concordant dysregulation of EGR1, PFKFB3, HDAC4, MMP13 and PDK4 was observed at both mRNA and protein levels in human OA synovium and DMM mouse joints. Conclusion: This comprehensive analysis identified acetylation-related genes and analyzed their potential biological roles in OA. The identified ARDEGs may provide new insights into OA diagnosis and treatment. Full article

Osteoarthritis is an irreversible degenerative joint disease driven by sustained NF-κB-mediated inflammatory responses, and conventional intra-articular hyaluronic acid or small-molecule NF-κB inhibitors cannot achieve targeted on-demand treatment due to poor solubility, rapid clearance and lack of lesion microenvironment responsiveness. OA with inherent anti-chondrolytic activity can self-assemble into nanocarriers in water, yet it lacks stimuli-responsive capacity. Herein, we rationally designed and synthesized an OA-Der by covalently conjugating o-phenylenediamine fragments to the OA backbone. ¹H NMR and HRESI-MS spectra fully verified the accurate chemical structures of intermediate and final OA-Der. Blank OA-Der micelles exhibited uniform spherical core–shell nanostructures (50–150 nm) under TEM and AFM, while pathological high NO triggered complete disassembly of micellar assemblies. We further co-assembled OA-Der with NF-κB inhibitor BAY 11-7082 to construct NO-responsive BAY@OA-Der supramolecular micelles. In vitro experiments using human C28/I2 chondrocytes with LPS-induced inflammatory injury demonstrated that BAY@OA-Der significantly improved cell viability and reduced apoptotic chondrocyte proportion. At mRNA and protein levels, the supramolecular micelle formulation remarkably suppressed NF-κB p65 phosphorylation, downregulated cartilage-degrading ADAMTS5, and upregulated ACAN compared with free BAY or blank OA-Der. Collectively, this natural bioactive self-assembled NO-responsive delivery platform achieves synergistic anti-inflammatory and matrix-protective effects by precisely releasing drugs at NO-overexpressed osteoarthritis inflammatory sites and offers an in vitro design strategy for osteoarthritis responsive delivery systems. Full article

Background/Objectives: Chronic hyperglycemia drives gingival fibroblast dysfunction, disrupting extracellular matrix homeostasis and the migratory capacity required for wound healing, which contributes to increased periodontal susceptibility in diabetes. Ferulic acid (FA), a dietary phenolic compound with antioxidant and anti-inflammatory properties, has demonstrated wound-healing activity in various tissues; however, its effects on human gingival fibroblasts (HGFs) under hyperglycemic conditions remain unclear. This study investigated the effects of FA on HGF viability, wound closure, and the secreted concentrations of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1), and interleukin-6 (IL-6) under normoglycemic and hyperglycemic conditions. Methods: Cultured HGFs (HGF-1 cell line) were pre-conditioned for 72 h under normal glucose (5.5 mM) or high glucose (25 mM), with an iso-osmolar mannitol control to distinguish glucose-specific effects from osmotic changes. Viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and wound closure by scratch assay following FA treatment, while MMP-1, TIMP-1, and IL-6 concentrations in conditioned medium were quantified by enzyme-linked immunosorbent assay (ELISA). Results: FA was non-cytotoxic at all tested concentrations, whereas 50 µM transiently increased viability. FA significantly enhanced wound closure under both conditions, independent of osmotic effects. High glucose increased IL-6 concentration in the conditioned medium (significant at 48 h) and MMP-1 levels. FA partially attenuated MMP-1 levels at specific time points, modestly reduced IL-6 levels, and markedly increased TIMP-1 concentration under both glucose conditions. Conclusions: FA enhanced wound closure in scratch assay and shifted the secreted MMP-1/TIMP-1 concentration ratio toward a more favorable, matrix-protective profile at the protein level, without cytotoxicity, supporting further investigation of its potential role in periodontal tissue repair under high glucose conditions. Full article

Chronic inflammatory signaling contributes to cartilage degeneration across multiple joint diseases, yet the molecular consequences of sustained cytokine exposure remain incompletely understood. We investigated how prolonged interleukin-1β (IL-1β) stimulation remodels the chondrocyte proteome and whether these changes are associated with senescence-associated traits. Primary human articular chondrocytes were exposed to IL-1β (10 ng/mL) for up to four days. Time-resolved data-independent acquisition (DIA) proteomics was integrated with immunofluorescence, quantitative PCR, multiplex metalloproteinase profiling, BrdU incorporation, growth-curve analysis, and senescence-associated β-galactosidase assays. Sustained IL-1β induced extensive time-dependent proteomic remodeling, with early inflammatory and extracellular matrix responses followed by alterations in cell-cycle regulation and cytoskeletal organization. Prolonged stimulation was associated with persistent downregulation of CDK4, Cyclin D1, DNA replication-associated proteins, and Rho GTPase-associated components, accompanied by actin cytoskeletal remodeling. These molecular changes were associated with impaired proliferation, increased senescence-associated β-galactosidase activity, and transient modulation of p21. Following cytokine withdrawal, BrdU incorporation showed partial recovery. Together, these findings indicate that sustained IL-1β progressively reshapes the chondrocyte cellular state through coordinated remodeling of proliferative, cytoskeletal, and metalloprotease programs while showing some degree of proliferative plasticity under the conditions tested. Full article

This study investigated the interactions between phenolic compounds from Israeli and Chilean white wines and human serum carrier proteins, including human serum albumin (HALB), gamma-globulin (HGLO), and fibrinogen (HFB), to characterize their antioxidant capacity and serum protein-binding behavior under controlled experimental conditions. The analyzed wines included Israeli Chardonnay (ICR), Chilean Chardonnay (CCR), Israeli Sauvignon Blanc (ISB), and Chilean Sauvignon Blanc (CSB). HPLC and FTIR fingerprinting revealed cultivar- and region-dependent differences in phenolic composition, with Chardonnay wines showing stronger protein-binding behavior and Sauvignon Blanc samples displaying high antioxidant efficiency relative to their phenolic content. ICR exhibited the highest total binding capacity, 46.44%, and the strongest albumin interaction, with a binding constant (Kb) of 8.44 × 10⁴ M⁻¹ and a Gibbs free energy (ΔG) value of −35.03 kJ/mol. Empirical fluorescence quenching kinetics demonstrated that white wine phenolics establish stable physical complexes with human serum proteins, displaying a distinct preferential affinity for HALB as the protein showing the strongest apparent interaction among the proteins tested. Two- and three-dimensional fluorescence spectroscopy confirmed substantial quenching of the intrinsic tryptophan and tyrosine residues, indicating meaningful microenvironmental alterations within the protein’s active transport sites. These empirical interactions were closely mirrored by complementary molecular docking simulations, which provided a structural visualization of the physical binding interactions. ICR also showed the highest antioxidant capacity, with DPPH and CUPRAC values of 1.66 and 2.91 mmol TE/L, respectively. Ethanol control showed negligible effects, indicating that the observed bioactivity was mainly associated with the polyphenolic matrix. Among the investigated samples, Chardonnay showed higher apparent protein-binding capacity, whereas Sauvignon Blanc showed relatively high antioxidant efficiency in relation to its phenolic content. Full article

The matrix metalloproteinases MMP-2 and MMP-9 are involved in extracellular matrix remodeling, inflammatory response, and tissue remodeling, and overactivity of certain metalloproteinases may also contribute to chronic wound healing. The aim of this work was to synthesize novel hybrid derivatives of orotic acid and 1,2,4-triazole and investigate them as potential modulators of MMP-2/MMP-9. The structure of the compounds was confirmed by ¹H, ¹³C NMR spectroscopy, LC–MS, and elemental analysis. Pharmacokinetic properties were calculated using SwissADME, and enzyme interactions were characterized using molecular docking strategies, protein–ligand contact analysis, and 100 ns molecular dynamics. The inhibitory effect was also assessed in vitro by fluorimetry at a concentration of 10 μM. The compounds had an acceptable drug-like profile, without violations of Lipinski’s rule and PAINS warnings. The highest affinity for MMP-9 was also found for the three target proteins 17, 19 and 13, which showed values of −9.65, −9.47 and −9.17 kcal/mol, respectively, compared to −8.37 kcal/mol for NNGH. Dynamic molecular analysis confirmed the stability of the 13–MMP-9 complex. Compounds 17 and 13 inhibited MMP-9 by 94.2 ± 4.8% and 85.2 ± 3.8%, respectively, with little effect on MMP-2, whereas compound 19 showed balanced inhibition of MMP-2 and MMP-9 by 74.2 ± 4.4% and 79.2 ± 2.8%, respectively. The results identified 13 and 17 as potential compounds with preferential effects on MMP-9, and 19 as a possible dual inhibitor for wound healing activity studies. Full article

Keratoconus (KC) is a degenerative corneal disease, characterized by stromal thinning and abnormal ECM remodeling, leading to fibrosis. Corneal fibrosis is a leading cause of visual impairment. Corneal stromal keratocytes differentiate into myofibroblasts, which alters extracellular matrix (ECM) protein deposition. Nintedanib (NIN) is an antifibrotic FDA-approved tyrosine kinase inhibitor, but its function in the cornea is largely unknown. This study examined the impact of NIN within the human corneal stromal microenvironment. Healthy corneal stromal fibroblasts (HCFs) and KC fibroblasts (HKCs) in 2D and 3D in vitro cultures were treated with 1 μM or 2.5 μM NIN. Cell types were evaluated in 2D cultures for metabolic activity, viability, and migration. Protein expression of alpha-smooth muscle actin (α-SMA), collagens (COLs) 1, 3, and 5, cellular fibronectin containing extra domain A (EDA-FN), and thrombospondin-1 (TSP-1) were evaluated in 3D cultures. NIN reduced metabolic activity in HKCs without affecting cell viability. NIN reduced cell migration, downregulated COL3, COL5, EDA-FN, and TSP-1 expression in HCFs and HKCs. COL1 was upregulated in HCFs, whereas α-SMA was upregulated in HKCs. Overall, these findings demonstrate that NIN modulates corneal stromal cell migration and fibrotic marker expression, highlighting its potential as a therapeutic strategy for reducing corneal fibrosis associated with keratoconus. Full article

Chinese distillers’ grains (CDGs) are a lignocellulose-rich agricultural byproduct with considerable bioconversion potential; however, their recalcitrant structure imposes a major bottleneck for efficient valorization. In this study, six white-rot fungal strains and two Trichoderma strains were isolated from wild macrofungi, among which Ganoderma sp. 2G1-6 exhibited the highest laccase activity, reaching 11.29 U/mL. Whole-genome sequencing revealed a 49.15 Mb genome containing 12,437 predicted proteins, including a substantial repertoire of 196 glycoside hydrolases and 113 auxiliary activity enzymes implicated in lignocellulose degradation. Solid-state fermentation of CDGs with Ganoderma sp. 2G1-6 produced high enzyme activities, including endoglucanase (13.3 ± 4.6 U/g), xylanase (538.8 ± 33.0 U/g), β-glucosidase (26,572 ± 2996 U/g), and laccase (231.2 ± 16.7 U/g). Concomitantly, the nutritional profile of CDGs was markedly improved after 30 days, with crude protein increasing by 28.51%, acid-soluble protein by 33.33%, and soluble dietary fiber by 159%. Complementary structural analyses (FTIR, SEM, XRD, and TGA) confirmed progressive disruption of the lignocellulosic matrix, selective delignification, and enhanced cellulose exposure. These findings establish Ganoderma sp. 2G1-6 as a promising microbial chassis for CDGs valorization and provide preliminary functional profiles of Ganoderma species for lignocellulose bioconversion. Full article

To investigate the effects of mulberry leaf extract (MLE) on the growth performance, organ indices, and flesh quality of grass carp (Ctenopharyngodon idella), a basal diet (Control, Crude protein 30.25%, Crude lipid 7.23%) and three MLE-supplemented diets containing 1%, 2%, and 4% MLE (MLE1%, MLE2%, MLE4%) were formulated. A total of 160 grass carp (259.7 ± 1.1 g) were randomly allocated into 16 cages (1 m × 1 m × 1.2 m), with 10 fish per cage and 4 replicate cages per treatment group. Throughout the 8-week feeding trial, juvenile grass carp were fed three times daily (08:00, 12:00, and 17:00) at a daily feeding rate of 1.5–2.0% body weight. At the end of the trial, growth performance was assessed. Additionally, four fish were randomly sampled from each cage to determine the organ indices, flesh quality parameters, and gene expression levels. In the results, the final average body weight of all groups ranged from 909.00 to 942.97 g, and all the groups exhibited no significant difference in growth performance (p > 0.05). MLE-supplemented groups had significantly decreased visceral somatic index and hepatic somatic index (p < 0.05). In terms of flesh quality, all MLE-supplemented groups increased the flesh shear force, springiness, whiteness, and lightness (p < 0.05). Compared with the Control group, the MLE4% group had increased flesh hardness, gumminess, and chewiness, from 2899.52 g, 1310.62, and 516.59 to 4122.99 g, 1958.48, and 887.76, respectively (p < 0.05). MLE significantly decreased the 48 h thawing loss (MLE2%), 96 h thawing loss (MLE1%, MLE2%, MLE4%), and flesh crude lipid content (MLE2%, MLE4%) (p < 0.05). In terms of collagen metabolism, compared with the Control group, MLE significantly increased the flesh collagen content (MLE2% and MLE4%) (p < 0.05), upregulated the expression level of La ribonucleoprotein 6 (MLE4%) and tissue inhibitor of metalloproteinase 1 (MLE4%). Matrix metallopeptidase 2 was significantly downregulated in all MLE-supplemented groups (p < 0.05). In terms of myofiber development, compared with the Control group, the myofiber density was higher, and the myofiber diameter was lower in all MLE-supplemented groups (p < 0.05). MLE significantly upregulated the expression level of mammalian target of rapamycin (MLE4%), musculoskeletal embryonic nuclear protein 1 (MLE4%), myogenic differentiation 1 (MLE2%, MLE4%), and myogenic factor 5 (MLE1%, MLE2%, MLE4%) (p < 0.05). Myotubularin-related protein 8 was significantly downregulated in all MLE–supplemented groups (p < 0.05). In conclusion, dietary supplementation with 2–4% MLE improves the flesh textural properties, chroma and water-holding capacity of grass carp. MLE improves the flesh quality of grass carp by enhancing collagen deposition and myofiber development. Full article