Existing deep learning strategies for identifying bioactive peptides (BAPs) are often limited by single-task models and shallow sequence-based features, which restricts their generalizability. This study introduced an autoencoder based deep learning framework (BioPepAE) that leverages peptide atomic 3D information from AlphaFold 3 to enable recognition of multiple types of BAPs, including anti-hypertensive peptides (AHPs), antioxidant peptides (AOPs), and anti-aging peptides (AAPs). BioPepAE achieved high accuracy (94.65% for AHPs, 95.47% for AOPs, 92.86% for AAPs) and demonstrated strong generalization on independent tests. BioPepAE identified 8 AHPs, 13 AOPs, and 5 AAPs from wheat germ protein hydrolysates, and subsequent in vitro assays confirmed the bioactivity of randomly selected peptides, thus validating its predictive accuracy and practical utility. Moreover, BioPepAE requires no complex parameter tuning for identifying different BAPs. This study presents a robust and versatile framework for the universal and accurate identification of BAPs by integrating 3D structural information with deep learning.

Hypertrophic cardiomyopathy (HCM) and hypertension often coexist, sharing common etiological factors and pathological mechanisms. Both traditional and modern medicine have explored food and medicine products for their treatment This study examines the therapeutic potential and mechanisms of Achyranthis bidentatae radix and Saururus chinensis, two natural products used in food and medicine homology, in addressing HCM and hypertension. Bioinformatics and computer-aided drug design (CADD) approaches were utilized to identify active ingredients and mechanisms. In vivo and ex vivo experiments were performed to validate the pharmacological effects under conditions mimicking HCM and hypertension. Disease-related genes were identified using GeneCards and DisGeNET, while key components were identified via Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). A total of 62 disease-related genes were identified, with 20 significant components for A. bidentatae radix and 5 for S. chinensis Intersection analysis highlighted 18 common target genes involved insulin-like growth factor 1 receptor (IGF1R), insulin receptor (INSR), insulin (INS), Matrix Metallopeptidase 9 (MMP9), signal transducer and activator of transcription 3 (STAT), were confirmed through real-time PCR in vivo. Molecular docking studies demonstrated direct interactions between quercetin and IGF1R, INSR, MMP9, and between inophyllum E and INS. Molecular dynamics simulations showed favorable binding of quercetin with INSR. Quercetin exhibited promising drug-likeness and therapeutic potential in angiotensin II-treated cardiomyocytes. In conclusion, quercetin, identified as active component in A. bidentatae radix and S. chinensis, shows promising therapeutic effects against HCM and hypertension. These findings highlight the potential of these natural products in cardiovascular disease management through targeted molecular interactions. Future research should explore the nature products with long-term effects in comprehensive cardiovascular disease treatment.

Food and medicine homologous(FMH)products provide enhanced safety and tolerability.This study aimed to identify functional FMH compounds against cardiac hypertrophy.Bioinformatics analysis and in vivo experiments were utilized to pinpoint key genes in cardiac remodeling.A functional component screening was performed using the FMH compound database(FMHCD),followed by an evaluation of drug-like properities.Pharmacological assessments included measures of cardiac function,cardiac hypertrophy and fibrosis determination,and mitochondrial function.Transcriptome analysis was carried out to explore potential mechanisms.Interaction studies involved luciferase reporter assays,chromatin immunoprecipitation(ChIP)assays,and loss-of-and gain-of-function verifications.NRF2 has been identified as a critical gene in cardiac remodeling.Among the FMHCD compounds,β-ecdysterone(β-Ecd)was the most promising NRF2 enhancer,showing dose-dependent effectiveness in reversing cardiac remodeling.High concentration of β-Ecd resulted in approximately a 2.15-fold improvement.Downregulation of NRF2 negated the beneficial effects of β-Ecd,increasing cardiac hypertrophy by roughly 2.14-fold,oxidative stress by 1.94-fold,and mitochondrial dysfunction by 1.69-to 2.14-fold.Slc41a3 was identified and confirmed as being directly regulated by NRF2.Under AngⅡ stimulation,knockdown of Slc41a3 in cardiomyocytes reduced mitochondrial oxidative stress by 87.9％and mitochondrial dysfunction by 1.8-fold.Overexpression of Slc41a3 counteracted the protective effects of β-Ecd,elevating mitochondrial oxidative stress by approximately 1.75-fold and impairing mitochondrial function by 1.75-to 2.93-fold in cardiomyocytes.β-Ecd alleviates cardiac hypertrophy via the NRF2/Slc41a3 pathway,regulating oxidative stress and mitochondrial dysfunction.

Natural polysaccharide-based hydrogels have emerged as important material platforms in food science and biomedical research; however, the roles among polymer structure, metal ions, and nanomaterials in determining network formation and printability remain insufficiently understood in an integrated framework. This review systematically examines six representative polysaccharides (chitosan, alginate, starch, pectin, hyaluronic acid, and chondroitin sulfate), with emphasis on how their different functional groups govern ion-mediated crosslinking, nanomaterial incorporation, and the synergistic regulation of hydrogel properties. The reviewed literature indicates that these interactions directly affect gelation behavior, mechanical integrity, and functional performance. In the specific context of extrusion-based 3D printing, these factors collectively regulate the critical balance among shear thinning, post-extrusion recovery, and shape fidelity. As a result, these hydrogels have been applied in printed food systems, packaging, tissue engineering, wound dressings, drug delivery, and flexible sensors. The accumulated evidence indicates that successful hydrogel design requires the coordinated consideration of polysaccharide structure, metal-ion interactions, and nanophase reinforcement, rather than reliance on any single modification strategy. Further development will require standardized printability metrics, rigorous evaluation of post-printing stability under end-use conditions, consistent reporting of key material and processing parameters, and robust safety evidence to support practical applications.

Panax ginseng, a foundational herb in traditional East Asian medicine, has been extensively studied for its therapeutic and nutritional properties. Among its bioactive constituents, ginseng polysaccharides (GPs) stand out for their potent antioxidant, anti-inflammatory, and immunomodulatory effects. These polysaccharides, primarily composed of monosaccharides such as glucose, galactose (Gal), and arabinose (Ara), demonstrate promising potential in alleviating oxidative stress and immune suppression. With increasing exposure to ionizing radiation from medical and industrial sources, the demand for effective radioprotective agents has grown. Ionizing radiation induces DNA damage and excessive reactive oxygen species (ROS) production, resulting in oxidative stress and immune dysfunction. Research suggests that GPs mitigate radiation-induced cellular damage by enhancing antioxidant enzyme activity, suppressing inflammatory cytokines, and regulating immune responses. Despite these encouraging findings, further investigations are needed to elucidate their mechanisms of action and optimize their clinical applications. This review provides a comprehensive analysis of the composition, biological activities, and radioprotective mechanisms of GPs, highlighting their potential as functional agents for safeguarding human health against radiation-induced damage.

BACKGROUND AND PURPOSE:Emodin inhibits cardiac fibrosis through metastasis-associated protein 3 (MTA3), but its limited bioavailability hinders clinical application. To enhance emodin's clinical potential, a new derivative, emodin succinyl ethyl ester, was synthesised by modifying the 3'-OH position. This study assessed its drug-likeness, anti-fibrotic properties and molecular mechanisms involving MTA3. EXPERIMENTAL APPROACH:Drug-likeness properties of the emodin derivative were evaluated using computational-aided drug design (CADD). Transverse aortic constriction (TAC)-induced cardiac fibrosis and Angiotensin II (Ang II)-stimulated cardiac fibroblasts were used in vivo and ex vivo, respectively, to determine the effects of the emodin derivative on cardiac fibrosis and fibroblast transdifferentiation. Bioinformatics analysis, CADD, chromatin immunoprecipitation (ChIP), luciferase reporter assays and functional experiments were employed to predict, identify and validate the relationship between MTA3 and its upstream transcription factors. KEY RESULTS:The emodin derivative exhibited superior drug-likeness and anti-fibrotic effects compared to emodin by effectively inhibiting cardiac fibroblast transdifferentiation and restored MTA3 expression. E2F1 was identified and validated as a transcriptional regulator, promoting α-SMA and COL1A2 expression, and directly reducing MTA3 expression in cardiac fibroblasts. The emodin derivative demonstrated stronger binding to the E2F1 transcription site than emodin, reducing E2F1 expression and enhancing anti-fibrotic action. CONCLUSIONS AND IMPLICATIONS:The emodin derivative shows improved drug-likeness and potent inhibition of cardiac fibrosis by targeting E2F1, disrupting its pro-fibrotic function, restoring MTA3 expression and halting fibrosis progression. This advances emodin derivative's potential as a clinical therapy for cardiac fibrosis and provides insights into its anti-fibrotic mechanisms.

BACKGROUND:Sleep deprivation (SD) is a significant public health concern and a risk factor for neuropsychiatric disorders, including depression. SD disrupts the gut-brain axis, causing dysbiosis and neuroinflammation. Astragalus membranaceus (AST) exhibits antidepressant and anti-inflammatory properties, including modulation of the gut microbiota; however, its neuroprotective effects on SD-induced neuropsychiatric disturbances remain largely unexplored. This study investigates the potential of AST using an innovative integrative multiomics approach. PURPOSE:This study was conducted to investigate the neuroprotective effects of AST against SD-induced depression-like behavior and to explore the mechanism underlying its regulatory effects on the gut-brain axis. METHODS:We established a chronic SD mouse model that was subjected to AST intervention and employed a pioneering integrative multiomics approach-combining resting-state functional magnetic resonance imaging for brain function, metagenomics for microbiota profiling, metabolomics for metabolic alterations, and transcriptomics for gene expression in key brain regions. Behavioral tests and cytokine assays complemented these analyses to comprehensively evaluate the therapeutic effects of AST. RESULTS:SD induced depression-like behavior, neuroinflammation (IL-1β, IL-6, and TNF-α secretion), gut dysbiosis (Proteobacteria expansion, loss of beneficial microbes), and disrupted metabolic pathways. AST alleviated behavioral deficits, normalized brain connectivity, and reduced the levels of proinflammatory cytokines. It also reshaped microbiota, enriching Muribaculum and Butyricicoccus, and restored metabolic profiles, increasing the levels of short-chain fatty acids and promoting bile acid pathways. Integrated analysis linked microbiota restoration to reduced neuroinflammation and improved neuroprotection. CONCLUSION:AST modulates the gut-brain axis to counteract SD-induced dysbiosis, neuroinflammation, and metabolic imbalance, alleviating depression-like symptoms. These findings offer novel mechanistic insights into the therapeutic potential of AST for SD-related neuropsychiatric conditions.

Complicated relationships exist among lifestyles, gut microbiome (GM), and human health. Lifestyles can modulate the composition and function of GM, hence influencing the development of non-communicable diseases (NCDs). Recently, the socio-economic growth in China has led to the emergence of urbanized lifestyles, including unbalanced eating patterns and a sedentary lifestyle, causing an increased incidence of lifestyle-related NCDs among the Chinese population. In this review, we discussed the impact of lifestyle specific to the Chinese population on the GM and highlighted the mechanistic evidence that the commensals and their metabolites prevent or promote the pathogenesis of common lifestyle-related NCDs in China. Additionally, we described several microbiome-targeted therapies derived from traditional Chinese health practices, including traditional Chinese medicine treatments, the intake of fermented foods and tea, and Tai Chi intervention. In conclusion, we emphasized the significance of lifestyle-induced dysbiosis in the etiology of prevalent NCDs in China and provided relevant solutions, which should offer new insight into the treatment of these diseases to improve the overall health status of Chinese citizens.

BackgroundMacrophage polarization plays a pivotal role in shaping the tumor microenvironment and influencing cancer progression. Long non-coding RNAs (lncRNAs) have emerged as important regulators of this process. This study investigated the role of lncRNA OIP5-AS1 in lung adenocarcinoma (LUAD) progression and its involvement in macrophage polarization.MethodsThe expression of OIP5-AS1 in LUAD tissues and its association with patient prognosis were analyzed. Functional assays, including cell proliferation, migration, invasion, and cell cycle analysis, were conducted in LUAD cell lines. Bioinformatics prediction, luciferase reporter assays, and RNA immunoprecipitation (RIP) were used to explore the interaction among OIP5-AS1, miR-429, and DOCK4. Macrophage polarization and migratory capacity were assessed following manipulation of OIP5-AS1, miR-429, and DOCK4 expression.ResultsOIP5-AS1 expression was significantly decreased in LUAD tissues and associated with poor survival. Overexpression of OIP5-AS1 inhibited LUAD cell proliferation, migration, and invasion, induced G1 phase arrest, and suppressed tumor growth in vitro. Mechanistically, OIP5-AS1 functioned as a molecular sponge for miR-429, regulating DOCK4 expression. Overexpression of miR-429 or knockdown of DOCK4 reversed the effects of OIP5-AS1 on macrophage polarization markers and restored macrophage migration.Conclusion:OIP5-AS1 modulates macrophage polarization through the miR-429/DOCK4 axis and inhibits LUAD cell progression. This regulatory pathway may influence the tumor immune microenvironment and represent a potential therapeutic target in LUAD.

Space flight has many adverse effects on the physiological functions of astronauts. Certain similarities have been observed in some physiological processes of rodents and astronauts in space, although there are also differences. These similarities make rodents helpful models for initial investigations into space-induced physiological changes. This study uses a 3D-Clinostat to simulate microgravity and explores the role of microgravity in space flight-induced liver and brain abnormalities by comparing changes in the gut microbiota, serum metabolites, and the function and physiological biochemistry of liver and brain tissues between the simulated microgravity (SMG) group mice and the wild type (WT) group mice. The study, based on hematoxylin-eosin (HE) staining, 16S sequencing technology, and non-targeted metabolomics analysis, shows that the gut tissue morphology of the SMG group mice is abnormal, and the structure of the gut microbiota and the serum metabolite profile are imbalanced. Furthermore, using PICRUST 2 technology, we have predicted the functions of the gut microbiota and serum metabolites, and the results indicate that the liver metabolism and functions (including lipid metabolism, amino acid metabolism, and sugar metabolism, etc.) of the SMG group mice are disrupted, and the brain tissue metabolism and functions (including neurotransmitters and hormone secretion, etc.) are abnormal, suggesting a close relationship between microgravity and liver metabolic dysfunction and brain dysfunction. Additionally, the high similarity in the structure of the gut microbiota and serum metabolite profile between the fecal microbiota transplant (FMT) group mice and the SMG group mice, and the physiological and biochemical differences in liver and brain tissues compared to the WT group mice, suggest that microgravity induces imbalances in the gut microbiota, which in turn triggers abnormalities in liver and brain metabolism and function. Finally, through MetaMapp analysis and Pearson correlation analysis, we found that valeric acid, a metabolite of gut microbiota, is more likely to be the key metabolite that relates to microgravity-induced gut microbiota abnormalities, disorders of amino acid and lipid metabolism, and further induced metabolic or functional disorders in the liver and brain. This study has significant practical application value for deepening the understanding of the adaptability of living organisms in the space environment.

Cardiac fibrosis is a pathological hallmark of various cardiovascular disorders. Accumulating evidence has demonstrated that fibroblasts transform into myofibroblasts during the occurrence of cardiac fibrosis, but the mechanism remains incompletely understood. This study aims to investigate the relevance of MTA3 as a potential therapeutic target for cardiac fibrosis. The myocardial infarction model was established by ligating the left coronary artery of C57BL6 mice, and myocardial fibrosis was measured by cardiac ultrasound and Sirius red staining of myocardium. MTA3 overexpression plasmid was constructed and transfected into primary fibroblasts, immunofluorescence, Western blot and qRT-PCR were used to detect the expression of MTA3, α-SMA, and Collagen I. RNAi was used to interfere with the downstream potential target gene E2F1. SB203580, a specific inhibitor of p38 MAPK, reduced the levels of phosphorylated p38 MAPK (p-p38) by inhibiting p38 MAPK activity, and allowed assessment of MTA3-induced fibroblast to myofibroblast transformation. The expression of MTA3 was reduced in fibrotic myocardium. Overexpression of MTA3 could restore cardiac function. During the transformation process of cardiac fibroblasts into myofibroblasts, the expression of MTA3 was downregulated. After overexpression of MTA3, the mRNA and protein levels of α-SMA and Collagen I were significantly reduced. When E2F1 was disrupted, the mRNA and protein levels of α-SMA and Collagen I were downregulated. Inhibition of p-p38 MAPK expression by SB203580 ameliorated myocardial fibrosis. MTA3 regulates the transformation of fibroblast into myofibroblast by p38 MAPK-E2F1 signaling pathway, and MTA3 may become a potential target for treating cardiac fibrosis.

Cannabidiol (CBD), a non-psychotropic compound derived from Cannabis sativa, has garnered attention as a potential therapeutic agent for various neurodegenerative diseases, including Alzheimer's disease (AD). Despite growing interest, additional research is required to clarify the specific mechanisms by which CBD influences the pathological accumulation of β-amyloid (Aβ) associated with AD. Moreover, the interactions between CBD and the endocannabinoid system (ECS), both in the presence and absence of Aβ expression, remain a subject of active investigation. Elucidating these mechanisms may provide valuable insights for advancing both our understanding and the development of targeted interventions in neurodegenerative disease management. Using a multifaceted approach that integrates pharmacological interventions, immunofluorescence imaging, flow cytometry, and biochemical assays, we examined the effects of CBD on Aβ40 and Aβ42. Additionally, we analyzed the modulation of cannabinoid receptor 1(CB1 receptor) and fatty acid amide hydrolase (FAAH) in the presence or absence of Aβ expression, uncovering the intricate regulatory mechanisms of CBD. Our findings indicate a nuanced response to CBD; while it may produce side effects in non-pathological cells, it demonstrates an ability to induce autophagy and apoptosis in Aβ-expressing cells via the activation of the Microtubule-associated protein 1 light chain 3 B(LC3B) and Caspase-3 pathways. Furthermore, our investigation into faah-1 involvement highlighted its role in alleviating pharyngeal dysfunction and counteracting weight loss in Aβ-expressing Caenorhabditis elegans(C. elegans) strains. These insights advance our understanding of CBD's therapeutic potential in addressing neurodegenerative pathologies.

Inflammatory conditions are key mediators in the progression of various diseases. Silymarin, derived from Silybum marianum seeds and fruits, has shown efficacy in treating a range of liver diseases. The expanding corpus of research on silymarin highlights its promising role in preventing and managing inflammatory conditions and autoimmune without adverse effects. This review discusses the absorption, metabolism, and anti-inflammatory mechanisms of silymarin, exploring its impact on the secretion of inflammatory factors, such as nuclear factor kappa B (NF-κB) pathway, mitogen-activated protein kinase (MAPK) pathway, and antioxidant pathway. We delve into its disease-modifying potential for clinical applications, thereby laying a theoretical foundation for further silymarin research and clinical studies.

Exploring feasible drugs for the treatment of pathological cardiac hypertrophy has always been a focus of cardiovascular disease research. Paeoniflorin (PF) and β-Ecdysterone (β-Ecd) are the main active components of Paeonia lactiflora and Achyranthes bidentata, which can be used for the treatment of cardiovascular diseases, but their mechanism of action remains unclear. This study focused on oxidative stress and ferroptosis to investigate the protective effects of PF and β-Ecd on cardiac hypertrophy in primary cardiomyocytes and C57BL/6 mice, utilizing the integration of CCK8 assays, ros detection, molecular docking, real-time quantitative PCR, western blot, immunofluorescence, etc. The result of combination indices demonstrated a significant synergistic protective effect of PF and β-Ecd on cardiac hypertrophy. Furthermore, in vitro and in vivo studies further showed that the combination of PF and β-Ecd could improve the abnormalities of cell surface area, ANP, β-MHC, MDA, SOD, calcium ion, mitochondrial membrane potential and so on induced by cardiac hypertrophy through the inhibition effects of oxidative stress and iron metabolism, which might be closely related to the impact on the Nrf2/HO-1 and SLC7A11/GPX4 pathways. Altogether, this work revealed the mechanism of the combination of PF and β-Ecd in the treatment of cardiac hypertrophy from the aspects of suppressing oxidative stress and ferroptosis, aiming to promote effective treatment of the disease and the clinical application of PF and β-Ecd.

Background: SLC30A5, a member of the solute transporter protein family, is implicated in tumorigenesis and cancer progression. This study aimed to explore the expression and prognostic significance of SLC30A family genes in pan-cancer, with a specific emphasis on SLC30A5 in hepatocellular carcinoma (HCC). Methods: Expression patterns and prognostic implications of SLC30A family genes were assessed across 33 cancer types, especially HCC. Co-expression analysis explored the relationship between SLC30A5 and immune cell infiltration, immune checkpoints, pathway molecules related to tumor angiogenesis and epithelial-mesenchymal transition (EMT). The role of SLC30A5 in HCC was evaluated through in vitro and in vivo assays, including CCK8 viability assay, EdU cell proliferation assay, colony formation assay, apoptosis assay, wound healing assay, transwell migration assay, and xenograft mouse model assay using Huh7 cells with targeted knockdown of SLC30A5. Results: SLC30A family genes exhibited overexpression in various tumors. In HCC, upregulation of SLC30A5 expression correlated with adverse prognosis. Significant associations were observed between SLC30A5 expression and immune cell infiltration, immune checkpoints, molecules involved in angiogenesis, and EMT. SLC30A5 overexpression was associated with advanced disease stages, higher histological grades, and vascular invasion. Single-cell RNA sequencing data (GSE112271) revealed notable SLC30A5 expression in malignant cells. In vitro and in vivo assays demonstrated that SLC30A5 knockdown in Huh7 cells reduced proliferation, migration, and invasion while promoting apoptosis. Conclusions: This study highlights the clinical relevance of SLC30A5 in HCC, emphasizing its role in cell proliferation and migration. SLC30A5 emerges as a promising candidate for a prognostic marker and a potential target in HCC.

Traditional Chinese Medicine (TCM) formulations serve as a multi-component pharmacological combination therapy with various potential targets and have collected extensive knowledge regarding the in vivo efficacy of treating cardiovascular disorders in clinical practice for thousands of years. However, the obscurity of the chemicals and the molecular mechanisms are impediments to their continued growth and globalization. Therefore, new modern medications based on the combination of beneficial TCM components with precise clinical efficacy are required. The goal of this study was to find the best combination of Achyranthes bidentata Blume (AB) and Paeonia lactiflora Pall. (PL) for hypertension with liver yang hyperactivity (HLYH). The integrated research consisting of principal component analysis (PCA), metabolomics, microbiology, and weighted correlation network analysis (WGCNA) were used to find the optimal combination of AB-PL combinations and reveal the mechanism of action. The result showed AB-PL (2:3) had a substantial protective impact on HLYH, as shown by lower blood pressure, improved liver yang hyperactivity, reduced cardiac remodeling and malondialdehyde (MDA), and increased NO content. Furthermore, the essential elements for AB-PL reducing hypertension may be related to 135 metabolites and 23 microorganisms. In conclusion, our findings support the efficacy of herbal remedies in the treatment of hypertension and provide some pharmacological evidence for the ongoing development of novel modern Chinese drugs for cardiovascular disorders.

Background Medicine and food homological (MFH) products exhibit enhanced safety and tolerability, minimizing notable side effects, making them pivotal for prolonged use in cardiovascular diseases. This study aims to identify functional compounds in MFH based on cardiac remodeling-related target, employing reliable, comprehensive, and high-throughput methods.Methods By bioinformatics and in vivo verifications, we initially investigated the key target in the progression of cardiac remodeling. Subsequently, we performed molecular docking among medical homology compound database (MHCD), and then performed drug-likeness evaluations to recognize functional component based on disease-related target. Pharmacological verifications and data mining including cardiac and medullary transcriptomics, neurotransmitter metabolomics, resting-state functional magnetic resonance imaging (rs-fMRI), and correlationship analysis were utilized to define the benefical effects of MFH functional components, as well as its in-depth mechanims.Results The critical roles of oxidative stress and the key target of NRF2 in cardiac remodeling were discovered, and β-ecdysterone was screened as the most promising NRF2 enhancer in MHCD. Dose-dependent efficacy of β-ecdysterone in countering oxidative stress and ameliorating cardiac remodeling were then verfied by in vivo and ex vivo experiments. By data mining, the crosstalk mechanism between cardiac remodeling and neuromodulation was identified, and further unveiled Slc41a3 as a potential key factor influenced by β-ecdysterone. Additionally, β-ecdysterone mitigated increases in norepinephrine (NE) and its metabolites DHPG in the sympathetic nerve center hypothalamic paraventricular (PVN), as indicated by rs-fMRI. Cardiac and medullary transcriptomes revealed central-peripheral regulation signaling pathways during cardiac remodeling with the involvement of core gene of Dhx37 .Conclusions Our study identified β-ecdysterone as a natural MFH functional compound countering cardiac remodeling by targeting NRF2 elevation. It elucidates crosstalk between cardiac remodeling and neuromodulation, facilitating precise drug screening and mechanistic insights, providing substantial evidence for β-ecdysterone application and molecular mechanisms in cardiovascular diseases.### Competing Interest StatementThe authors have declared no competing interest.