The structural characterization of glycopeptides is essential for elucidating their functional activity. In this study, the glycopeptide structures of chicken egg yolk proteins were identified comprehensively. Glycopeptides were obtained from egg yolk via trypsin digestion followed by hydrophilic interaction chromatography enrichment. Intact N- and O-glycopeptide structures of egg yolk proteins were analyzed using glycoproteomics techniques, and their potential functional activities were subsequently investigated. A total of 424 N-glycopeptides and 306 O-glycopeptides were identified, corresponding to 48 N-glycosites on 37 N-glycoproteins and 39 O-glycosites on 25 O-glycoproteins, respectively, demonstrating the extensive heterogeneity of glycosylation modifications. Twenty-two egg yolk glycoproteins were concurrently modified by N- and O-glycosylation. The identified glycopeptides exhibited diverse oligosaccharide chain compositions, demonstrating macro- and micro-heterogeneity. Apolipoprotein B yielded the most abundant glycopeptide structures, comprising 130 N-glycopeptides and 62 O-glycopeptides. N-glycoproteins were significantly enriched in immune-related signaling pathways, such as lysosome and regulation of actin cytoskeleton, whereas O-glycoproteins were significantly enriched in the spliceosome signaling pathway. These findings elucidated the structural characteristics of glycopeptides derived from egg yolk proteins and provided a theoretical basis for investigating their functional activities and potential applications as functional food ingredients.

Developing oral nanoparticles (NPs) that combine anti-inflammatory effects with gut microbiome modulation enables an effective strategy for integrated ulcerative colitis (UC) therapy. Yet, the complex and dynamically evolving nature of the gastrointestinal milieu presents formidable challenges to the consistency and specificity of NP interventions. To address this challenge, this study designed and developed gastrointestinal microenvironment-adaptive NP via self-assembly, utilizing curcumin (Cur) for anti-inflammatory effects and anthocyanin (Cy) for microbiome regulation to achieve dual functional therapeutic outcomes. Employing the esterification strategy, hydroxypropyl-β-cyclodextrin (HPCD) was modified using citric acid (CA) and sulfonic acid (SA) to synthesize CACD (CA-modified HPCD) and SACD (SA-modified HPCD), respectively, which self-assembled in the presence of quaternary ammonium chitosan (HTCC), Cur, and Cy to yield NPs. NPs demonstrated high Cur encapsulation efficiency (EE) and encapsulation capacity (EC) across pH 2.0-7.0, highlighting their high gastrointestinal adaptability. In vivo experiments showed clear amelioration of colitis symptoms, including downregulation of pro-inflammatory cytokines and attenuation of tissue damage. HTCC-Cy-CACD-Cur NPs enriched Eubacterium siraeum_group and Prevotellaceae, HTCC-Cy-SACD-Cur NPs favored Peptococcus expansion, potentially contributing to improved immune regulation and attenuation of UC. These bifunctional NPs offer innovative UC therapy and precision nutrition interventions.

Bioactive peptides are emerging as promising candidates for therapeutic wound repair due to their potent wound-healing activity. However, in the complex wound microenvironment, they face drawbacks, including degradation, rapid clearance, and short duration of action, which limit their sustained healing efficacy. As functional carriers, hydrogels can enhance the therapeutic efficacy of bioactive peptides by preserving their activity, maintaining local concentrations, controlling the release behavior, and providing a three-dimensional microenvironment. This Review summarizes the latest advances in bioactive peptide-loaded hydrogels for wound repair. First, we review the sources of wound-healing peptides and then explain how hydrogel-mediated delivery, through mechanisms such as the protection of bioactivity and controlled release, has, to some extent, overcome the limitations of applying peptides directly to wounds. Additionally, we summarize several loading strategies and present the applications of these hydrogels for promoting acute and chronic wound repair. We conclude with research directions and future perspectives, aiming to provide references for further studies and clinical applications.

Hypoxia is a critical determinant in the etiology and progression of ischemic heart failure, but its underlying molecular mechanisms and regulatory interactions remain largely enigmatic. in our study, we employed differential analysis, coupled with WGCNA and the MSigDB database, to identify nine genes associated with hypoxia in heart failure. GO and KEGG enrichment analyses indicated that these genes are predominantly involved in hypoxia, immune responses, inflammation, apoptosis, and aging processes.Employing Bayesian networks, we elucidated four regulatory relationships among the hypoxia genes: PIM1-CDKN1A, IL6-CDKN1A, PLIN2-ANGPTL4, and SERPINE1-PLAUR. We amalgamated 12 machine learning algorithms, comprising 113 distinct combinations, to refine our findings and identified four pivotal hypoxia genes: SLC2A1, PLIN2, FOSL2, and PIM1. The SHAP analysis was instrumental in interpreting the predictive outcomes of the optimal model, the Random Forest algorithm, SLC2A1 was the most influential gene in the model. Immune infiltration analysis revealed the presence of seven types of dysregulated immune cells within the failing myocardium. Colocalization analysis showed that the posterior probabilities were predominantly concentrated on the gene-expression-only hypothesis and did not provide sufficient evidence for shared causal variants between the candidate-gene eQTL and HF GWAS signals. Overall, our research offers significant insights into the molecular mechanisms of hypoxia genes in the pathophysiology of heart failure, paving the way for the development of targeted and immunomodulatory therapies.

Iron is an essential trace element for maintaining normal physiological functions in living organisms. This study developed a novel iron supplementation strategy based on chelation reactions. Egg white peptides (EWPs) prepared by optimizing alkaline protease hydrolysis conditions (55 °C, 6 h, pH 10, etc.) possess abundant chelation sites, with relatively high levels of aspartic acid (10.53%) and glutamic acid (15.57%). Egg white peptides‑iron chelates (EWPs-Fe) were prepared via chelation reactions. The physical and chemical properties were characterized using methods such as FTIR. Finally, the application potential of the complexes was evaluated. The results indicate that EWPs-Fe primarily form stable chelates through coordinating groups such as carboxyl and amino groups. Compared to free peptides, EWPs-Fe (3:1) not only exhibits a smaller particle size and extremely low cytotoxicity-with a hemolysis rate below 5%-but also demonstrates significantly enhanced antioxidant activity. Findings indicate that EWPs-Fe combines excellent bioavailability with safety, offering a novel approach for iron supplement development.

Food-derived bioactive peptides (FDBPs), released from dietary proteins during processing, fermentation, or digestion, exhibit diverse physiological activities that are not fully explained by classical receptor- or enzyme-centered models. Depending on their amino acid composition, physicochemical properties, and assembly state, some FDBPs may interact directly with cellular membranes and modulate lipid organization. Membrane phase separation provides an emerging biophysical framework for interpreting the actions of FDBPs. This review presents a prospective analysis of FDBP-membrane phase interactions, emphasizing available research methods, biological contexts, and structure-activity relationships. In particular, we examine how peptide localization, charged and hydrophobic residues, chemical modification, and multivalent assembly may influence membrane fluidity, thickness, surface charge, and the organization of liquid-ordered and liquid-disordered domains. This perspective has the potential to broaden the mechanistic understanding of FDBPs' bioactivities and to guide the rational design of membrane-targeted functional foods.

Gastrointestinal barriers (acidic environment, mucus barrier, tight junctions, and microbiota metabolism) have long constrained the oral bioavailability of food-derived bioactives, especially lipophilic constituents. Recent advances in functionalized nanoparticle strategies offer sophisticated techniques to address these challenges. Specifically, precise control of particle size, morphology and surface functionalization enhances mucus penetration and cellular uptake of nanocarriers. Advanced nanocarrier strategies, such as mucosal adhesion, receptor-mediated targeting, and co-delivery with permeation enhancers, facilitate efficient absorption by opening intercellular gaps and activating specific endocytosis pathways. Intelligent designs for pH, enzyme, redox, and microbiome responses resulted in precise protection and targeted release of cargoes in various gastrointestinal segments. This review summarizes critical strategies for absorption-optimized oral nanoplatforms, including absorption mechanisms, mucosal retention, receptor-mediated endocytosis, co-delivery with absorption enhancers, and multi-strategy coupling. We emphasize strategic orientations for maximizing oral absorption efficiency of bioactive ingredients, offering a transformative framework for architecting next-generation oral nanocarrier platforms of food-derived components.

Hypoxia is a critical determinant in the etiology and progression of ischemic heart failure, but its underlying molecular mechanisms and regulatory interactions remain largely enigmatic. In our study, we employed differential analysis, coupled with WGCNA and the MSigDB database, to identify nine genes associated with hypoxia in heart failure. GO and KEGG enrichment analyses indicated that these genes are predominantly involved in hypoxia, immune responses, inflammation, apoptosis, and aging processes.Employing Bayesian networks, we elucidated four regulatory relationships among the hypoxia genes: PIM1-CDKN1A, IL6-CDKN1A, PLIN2-ANGPTL4, and SERPINE1-PLAUR. We amalgamated 12 machine learning algorithms, comprising 113 distinct combinations, to refine our findings and identified four pivotal hypoxia genes: SLC2A1, PLIN2, FOSL2, and PIM1. The SHAP analysis was instrumental in interpreting the predictive outcomes of the optimal model, the Random Forest algorithm, SLC2A1 was the most influential gene in the model.Immune infiltration analysis revealed the presence of seven types of dysregulated immune cells within the failing myocardium. Colocalization analysis suggested that hypoxia genes and heart failure are not likely to be independently influenced by the same genetic factors, although the potential for intermediary factors or shared biological pathways was not excluded.Overall, our research offers significant insights into the molecular mechanisms of hypoxia genes in the pathophysiology of heart failure, paving the way for the development of targeted and immunomodulatory therapies.

Food-derived exosomes (FEVs) are natural nanovesicles originating from dietary sources such as plants and milk. They exhibit excellent biocompatibility, low immunogenicity, and remarkable stability in the gastrointestinal tract, making them ideal carriers for colon targeted delivery of bioactive compounds. FEVs can encapsulate a wide range of therapeutic cargos including small interfering RNAs, small molecule drugs, and antibodies, and they possess inherent colon targeting properties. This review systematically summarizes the biological origins, isolation methods, and cargo loading strategies of FEVs, and highlights how their unique membrane composition and transmembrane transport mechanisms enhance stability, cellular uptake, and colon targeting efficiency. Emerging engineering strategies, such as surface modification, hydrogel encapsulation, and self-assembled, are discussed for further improving site specific delivery and therapeutic efficacy in inflammatory bowel disease and colorectal cancer. We also discuss key challenges for clinical translation, including standardization of isolation protocols, scalable production, and optimization of bioengineering approaches. Overall, this review emphasizes the potential of FEVs as intelligent and personalized nanomedicines for colon targeted therapy, providing a foundation for the development of next generation treatments for gastrointestinal diseases.

BackgroundThe progression of heart failure (HF) following myocardial ischemia/reperfusion (I/R) injury is driven by regulated cell death. Unlike the restrained nature of apoptosis, pyroptosis and necroptosis are lytic processes that trigger inflammatory cascades, causing extensive collateral damage to the non-regenerative myocardium. Understanding the integrated regulation of these pathways (PANoptosis) is essential for limiting infarct expansion.MethodsWe examined PANoptosis in rat I/R and H9c2 OGD/R models using transmission electron microscopy, immunofluorescence, and molecular markers (C-CASP3, N-GSDMD, p-MLKL). The functional hierarchy of the BIRC3-CASP8 axis was dissected using AAV-mediated gene transfer and pharmacological inhibitors.ResultsWe confirmed that I/R injury induces PANoptosis with interdependent crosstalk. Mechanistically, BIRC3 acted as a pivotal checkpoint: its upregulation inhibited CASP8, promoting membrane-rupturing pyroptosis and necroptosis. Crucially, BIRC3 silencing disinhibited CASP8, redirecting the cell death machinery toward apoptosis. This phenotypic shift preserved cell membrane integrity and minimized the release of inflammatory mediators, effectively halting the propagation of cell death to surrounding healthy cardiomyocytes.ConclusionsFor cardiomyocytes destined to die, the BIRC3-CASP8 axis serves as a decisive switch between destructive and silent death modes. By leveraging this axis to shift PANoptosis toward an apoptosis-dominant phenotype, we can reduce the inflammatory storm and collateral injury. This offers a promising therapeutic paradigm to maximize the preservation of functional myocardium and arrest HF progression.

Genistein (GEN) is the most abundant aglycone in soy isoflavones and is a key factor distinguishing soybeans from other food sources. It holds significant nutritional value and exhibits notable biological activity. However, the low water solubility of genistein limits its widespread application. To improve its water solubility, this study prepared gamma-cyclodextrin (gamma-CD)/GEN inclusion complexes and investigated their mechanism of action in alleviating hydrogen peroxide-induced oxidative stress damage in PC12 cells. The results showed that gamma-CD/GEN could be uniformly and stably dispersed in the system. Cell experiments indicated that gamma-CD/GEN significantly increased cell survival after treatment with organic hydrogen peroxide, and promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the expression of glutathione peroxidase 4 (GPx4). It also improved mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) levels, thereby alleviating cell damage caused by oxidative stress. Further Nrf2 knockdown experiments revealed that gamma-CD/GEN failed to provide protection, and no protective effect was observed under RSL3 intervention. In conclusion, gamma-CD/ GEN exerts antioxidant effects by activating the Nrf2/GPx4 pathway, thereby reducing oxidative stress damage induced by organic hydrogen peroxide, providing a theoretical basis for the development of novel antioxidants.

Background Despite maximal pharmacological treatment guided by clinical guidelines, the prognosis of heart failure (HF) remains poor, posing a significant public health burden. This necessitates uncovering novel pathological and cardioprotective pathways. Targeting cytokines presents a promising therapeutic strategy for HF, yet their intricate mechanisms in HF progression remain obscure. Methods HF datasets were obtained from the GEO database. Cytokine-related genes were identified through WGCNA and the CytReg database. GO and KEGG enrichment analyses were conducted using the clusterProfiler package. Reactome pathway enrichment analysis and Bayesian regulatory network construction were performed using the CBNplot package. Key genes were identified via LASSO regression and RF algorithms, with diagnostic accuracy evaluated by ROC curves. Potential therapeutic drugs were predicted using the DSigDB database, and immune cell infiltration was assessed with the CIBERSORT package. Results We identified 13 cytokine-related genes associated with HF. Enrichment analyses indicated these genes mediate inflammatory responses and immune cell recruitment. Bayesian network analysis revealed two cytokine regulatory chains: IL34-CCL5-CCL4 and IL34-CCL5-CXCL12. Machine learning algorithms identified five key cytokine genes: CCL4, CCL5, CXCL12, CXCL14, and IL34. The DSigDB database predicted 47 potential therapeutic drugs, including Proscillaridin. Immune infiltration analysis showed significant differences in seven immune cell types between HF and healthy samples. Conclusion Our study provides insights into cytokines' molecular mechanisms in HF pathophysiology and highlights potential immunomodulatory strategies, gene therapies, and candidate drugs. Future research should validate these findings in clinical settings to develop effective HF therapies.

Heart failure (HF) is a key public health concern worldwide due to its high morbidity and mortality rates. Calycosin (CA) is a flavonoid natural product that effectively treats HF with cardioprotective effects; however, its mechanism of action remains unclear. The present study aimed to investigate the therapeutic effect of CA on HF and its mechanism through in vivo and in vitro experiments, and to reveal the roles of pyroptosis and mitochondrial dysfunction in the pathophysiology of HF. The HF model was constructed 4 weeks after ligation of the left anterior descending artery in rats. Myocardial ischemia‑reperfusion injury was simulated using a hypoxia‑reoxygenation model and nuclear factor erythroid 2‑related factor (Nrf2) was silenced by transfection using small interfering RNA to further explore the therapeutic mechanism of CA. The results revealed that CA treatment improved cardiac function and myocardial injury, suppressed oxidative stress levels and improved mitochondrial ultrastructure in HF‑induced rats. CA downregulated the expression of relevant pyroptosis proteins via the Nrf2/reactive oxygen species (ROS)/thioredoxin‑interacting protein (TXNIP) pathway. In vitro experiments demonstrated consistent results confirming that CA ameliorated mitochondrial damage by reducing levels of ROS and inhibiting mitochondrial gasdermin D N‑terminal fragments activation. Silencing Nrf2 partially reversed the cardioprotective effects of CA, confirming the key therapeutic role of CA in Nrf2‑mediated anti‑pyroptosis. In conclusion, CA inhibits pyroptosis and improves mitochondrial damage in HF through the Nrf2/ROS/TXNIP pathway, which may disrupt the crosstalk between mitochondrial damage and pyroptosis, thereby exerting cardioprotective effects.

BACKGROUND:Calycosin (CA) is a flavonoid natural product that may effectively treats acute myocardial infarction (AMI), but its mechanism is unclear. METHODS:Targets related to AMI and CA were identified using the GEO database, SwissTargetPrediction, PharmMapper and literature searches. Protein-protein interactions analysis and Cytoscape were used to screen the core targets of CA for AMI treatment. Enrichment analysis identified biological pathways linked to AMI and potential mechanisms of CA. Immune infiltration analysis was used to explore the role of immune cells in AMI and the correlation between core targets and immune cells. And further validated in AMI rats with ligated left anterior descending. RESULTS:Bioinformatics identified relevant targets and biological mechanisms of AMI, and network pharmacology revealed 31 potential targets affected by CA, with NLRP3, IL-18, IL-1β, MMP9, and TLR4 as core targets. Enrichment analysis demonstrated the biological roles of these potential targets and NLRP3, IL1β and IL18 were selected for further analysis. Immune infiltration analysis showed that both NLRP3 and IL-1β were closely associated with monocytes, mast cells activated and neutrophils, and IL-18 was closely associated with monocytes. CA exerted cardioprotective effects in AMI rats by inhibiting NLRP3 inflammasome activation and reducing IL-18 and IL-1β levels, improving cardiac function and attenuating myocardial injury and fibrosis. CONCLUSION:CA effectively protects cardiac function and mitigates myocardial injury in post-AMI rats, probably through NLRP3 inflammasome inhibition.

ETHNOPHARMACOLOGICAL RELEVANCE:Heart failure (HF), the terminal stage of various cardiovascular diseases, represents a significant threat to global health. Fuxin Decoction (FXD), a classical Traditional Chinese Medicine (TCM) formula, has demonstrated therapeutic efficacy in HF treatment. However, its bioactive components and precise mechanisms remain to be elucidated. AIM OF STUDY:This study aimed to elucidate the material basis and mechanistic pathways underlying FXD's therapeutic effects on HF, thereby proposing a novel, safe, and effective treatment strategy. MATERIALS AND METHODS:First, UPLC-Q/TOF-MS was employed to identify active compounds in FXD. Subsequently, network pharmacology analysis was conducted to explore FXD's regulatory effects on ferroptosis and the Nrf2/SLC7A11/GPX4 signaling pathway. A rat HF model was established, and FXD's therapeutic effects were assessed via echocardiography and serum NT-proBNP measurement. Histopathological evaluation was performed using H&E and Masson staining, while mitochondrial ultrastructural changes were examined via transmission electron microscopy (TEM). Additionally, ferroptosis-related markers (Fe2+, MDA, GSH, and GPX4) were quantified in myocardial tissue. Finally, RNA interference-mediated Nrf2 silencing was applied to investigate FXD's cardioprotective effects and ferroptosis modulation in H9c2 cardiomyocytes. RESULTS:A total of 62 bioactive compounds were identified in FXD. Network pharmacology analysis revealed, for the first time, FXD's potential modulation of ferroptosis and the Nrf2/SLC7A11/GPX4 pathway. In vivo, FXD significantly improved cardiac function in HF rats, reduced NT-proBNP levels, and attenuated cardiomyocyte damage. FXD exerted potent anti-ferroptotic effects, evidenced by mitigated mitochondrial injury, decreased Fe2+ and MDA levels, and elevated GSH and GPX4 activity. Furthermore, FXD upregulated key proteins in the Nrf2/SLC7A11/GPX4 pathway. Crucially, Nrf2 silencing partially abolished FXD's cardioprotection, confirming Nrf2's central role in mediating FXD's anti-ferroptotic effects. CONCLUSIONS:FXD is a safe and effective therapeutic agent for heart failure, and its mechanism of action may be closely related to ferroptosis mediated by the Nrf2/SLC7A11/GPX4 signaling pathway.

Arginine demonstrates enhanced tissue repair capabilities, which may help alleviate intestinal barrier damage caused by pharmaceutical agents or other external factors. However, the intestinal barrier repair potential of arginine-terminated egg white peptides remains undetermined. In this study, we investigated the therapeutic effects of Leu-Phe-Arg (LFR) on dextran sulfate sodium (DSS)-induced intestinal barrier damage and elucidated its underlying mechanisms. Following 7-day DSS administration, damage models developed colitis manifestations including weight loss, rectal bleeding, and elevated disease activity index (DAI) scores. Therapeutic intervention with LFR demonstrated significant attenuation of oxidative stress, suppression of inflammatory mediators, and restoration of intestinal barrier integrity. Integrated transcriptomic and proteomic analyses revealed LFR's regulatory effects on colitis-associated pathways and amino acid metabolic networks. Notably, LFR administration downregulated key targets (PI3K, AKT, mTOR, and p70S6K) of the PI3K/AKT/mTOR/p70S6K signaling pathway. These findings provide novel mechanistic insights into the barrier-repairing properties of arginine-terminated bioactive peptides.

In this study, novel saltiness/saltiness enhancing peptides VESQTNGIIR, NQITKPNDVY, and DEDTQAMP were identified from the hen egg proteins via virtual enzymatic, molecular docking, and electronic tongue analysis. Their saltiness enhancement effect was analyzed by e-tongue analysis. Saltiness enhancement rates of saltiness peptide VESQTNGIIR were 47.24 %, 95.28 % and 105.94 %, and those of the saltiness peptide NQITKPNDVY were 32.40 %, 70.16 %, and 71.25 % at the salt reduction concentrations of 25 %, 35 % and 45 %, respectively. Saltiness enhancement rates of saltiness enhancing peptide DEDTQAMP were 5.83 % and 11.24 % at 25 % and 35 % salt reduction concentrations, respectively. Molecular docking demonstrated that Glu286, Arg330, Arg424, and Arg583 may be the key amino acids interacting with TMC4, whereas that carbon hydrogen bond, conventional hydrogen bond, and attractive charge interactions were important forces in peptides-TMC interactions. The study indicated that the peptides VESQTNGIIR and NQITKPNDVY may be ideal saltiness/saltiness enhancing peptides.

AIMS:Heart failure (HF) is an important public health problem worldwide, and programmed cell death (PCD) plays a crucial role in its pathologic process. This study aims to identify the hub genes associated with HF through PCD in order to better understand the pathogenesis of HF and improve its diagnosis and treatment. METHODS AND RESULTS:The gene expression dataset of HF was obtained from the GEO database. Bioinformatics and machine learning algorithms were utilized to screen the HF key genes and PCD-related HF hub genes, and an HF diagnostic model was constructed on this. Functional enrichment analysis clarified the gene ontology and signalling pathways of HF. The immune infiltration analysis of HF was performed to explore the expression levels of immune cells in each hub gene. Through bioinformatics analysis, 95 HF key genes were obtained. Functional enrichment analysis showed that they were mainly involved in inflammation, immunomodulation and other mechanisms. DHRS11 and LRKK2 were identified as PCD-associated HF hub genes by machine learning algorithms. The hub genes were confirmed as significant biomarkers of HF in the training and validation datasets, and their constructed nomogram had effective diagnostic value. Immune infiltration analysis showed significant immune imbalance of T-cell populations, monocytes and macrophages M2 in HF. CONCLUSIONS:In this study, DHRS11 and LRKK2 were identified as hub genes. HF diagnostic model construction and immune infiltration analyses were performed, which provided new ideas for the molecular mechanisms of HF development and treatment.

Acute myocardial infarction (AMI) and the myocardial ischemia-reperfusion injury (MI/RI) that typically ensues represent a significant global health burden, accounting for a considerable number of deaths and disabilities. In the context of AMI, percutaneous coronary intervention (PCI) is the preferred treatment option for reducing acute ischemic damage to the heart. Despite the modernity of PCI therapy, pathological damage to cardiomyocytes due to MI/RI remains an important target for intervention that affects the long-term prognosis of patients. In recent years, mitochondrial dysfunction during AMI has been increasingly recognized as a critical factor in cardiomyocyte death. Damaged mitochondria play an active role in the formation of an inflammatory environment by triggering key signaling pathways, including those mediated by cyclic GMP-AMP synthase, NOD-like receptors and Toll-like receptors. This review emphasizes the dual role of mitochondria as both contributors to and regulators of inflammation. The aim is to explore the complex mechanisms of mitochondrial dysfunction in AMI and its profound impact on immune dysregulation. Specific interventions including mitochondrial-targeted antioxidants, membrane-stabilizing peptides, and mitochondrial transplantation therapies have demonstrated efficacy in preclinical AMI models.

This study systematically elucidated the patterns of quality deterioration in egg yolk powder (EYP) during 60 days of accelerated storage under controlled conditions of (37 ± 0.5) °C and relative humidity maintained at (75 ± 5) %. The experiment found that with the extension of storage time, the sensory attributes and functional properties of EYP changed significantly: among the key functional indicators, solubility decreased by (39.02 ± 0.18) %, EAI decreased by (24.32 ± 1.79) %, and ESI increased by (50.02 ± 5.97) %. The internal water distribution showed characteristic phase changes. Large molecular lipid-protein complexes were formed internally. The analysis found that the synchronous oxidation of lipids and proteins is the core mechanism causing quality deterioration. By dynamically monitoring the changes in volatile substances, eight key differential volatile substances with stage-indicating functions were screened out. This conclusion provides theoretical support for the development of EYP with extended shelf life.