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. 2025 Dec 11;399(5):7433–7444. doi: 10.1007/s00210-025-04855-9

Integration of epidemiological surveys, network pharmacology, and molecular docking simulation to explore the potential key targets of propofol-induced euphoria

Linhong Wang 1,2,#, Zhongli Liao 3,#, Guanhua Qiu 1,2, Bin Yang 1,2,✉
PMCID: PMC13053373  PMID: 41379318

Abstract

Propofol is a widely used anesthetic that has been associated with post-anesthetic euphoria, particularly among women. Since anhedonia is a core component of female sexual dysfunction (FSD), we aimed to evaluate the clinical incidence of propofol-induced euphoria and explore its potential molecular mechanisms. A total of 300 patients undergoing gastrointestinal endoscopy with propofol anesthesia were assessed postoperatively using the Euphoria Rating Scale, Observer’s Assessment of Alertness/Sedation Scale (OAA/S), and the Hospital Anxiety and Depression Scale (HADS). Network pharmacology and molecular docking were applied to identify relevant molecular targets and signaling pathways. Euphoria occurred in 28% (42/150) of female patients compared to 4.4% (6/135) of males (adjusted OR = 6.62; 95% CI, 2.46 to 17.81, p < 0.001). Network pharmacology revealed 37 intersecting targets between propofol and FSD. Functional enrichment highlighted estrogen-related signaling and cGMP-dependent pathways. Molecular docking confirmed strong binding affinities of propofol with ESR1, EGFR, APP, NR3C1, MDM2, and MAOB. Short-term exposure to propofol can induce euphoria more frequently in females and may positively modulate pathways linked to female sexual dysfunction. These findings suggest propofol may have potential therapeutic applications beyond anesthesia.

Supplementary Information

The online version contains supplementary material available at 10.1007/s00210-025-04855-9.

Keywords: Propofol, Euphoria, Female sexual dysfunction, Estrogen pathway, Network pharmacology

Introduction

Female sexual dysfunction (FSD) affects approximately 40% of women in the USA, with 12% reporting distressing sexual problems. FSD is a progressive, age-related condition that can occur at any stage of life and is often associated with depression, anxiety, and other negative emotional states. In Asian countries, its prevalence is likely underestimated due to cultural suppression, limited treatment options, and a lack of specialists in female sexual medicine.

FSD manifests in various forms, including reduced sexual desire, impaired arousal, inability to achieve orgasm, and pain during intercourse. Among these, hypoactive sexual desire disorder (HSDD), characterized by persistent anhedonia and the absence of sexual fantasies, is particularly distressing and significantly impacts quality of life. Psychosocial stress and anxiety further exacerbate these symptoms, creating a bidirectional relationship between mental health and sexual function.

Propofol is one of the most widely used intravenous anesthetics, applied both in operating rooms and in procedural sedation outside surgery (e.g., dental, endoscopic, and MRI procedures) (Orchard and Heidari 2021). However, several reports have described unusual neuropsychiatric effects of propofol, including sexual hallucinations and post-anesthetic euphoria (Balasubramaniam and Park 2003; Brechmann et al. 2018; Kent et al. 1992; Marchaisseau et al. 2008; Martínez Villar et al. 2000; Uzbay and Shahzadi 2025; White and White 2023; Yang and Yi 2016). These phenomena appear to occur disproportionately in women, although cultural factors may influence reporting rates (Gwiazda et al. 2021). Despite these observations, the underlying mechanisms of propofol-induced euphoria and its potential relevance to FSD, particularly anhedonia, remain unclear.

In this study, we investigated the incidence of euphoria following propofol anesthesia in male and female patients undergoing gastrointestinal endoscopy. Furthermore, we employed a network pharmacology approach combined with molecular docking to identify potential molecular targets of propofol associated with FSD. By integrating clinical and molecular data, this study aims to investigate whether propofol induces euphoria through estrogen-related pathways, with the aim of providing potential therapeutic insights for FSD, particularly anhedonia.

Material and methods

Study design and ethical approval

This prospective observational study was conducted at the First Affiliated Hospital of Xiamen University between July 2024 and December 2024. The study protocol was approved by the institutional Ethics Committee (ID: XMFHIIT-2024SL336), and written informed consent was obtained from all participants in accordance with the Declaration of Helsinki.

Study population

A total of 300 adult patients (aged 18–55 years) scheduled for gastrointestinal endoscopy under propofol anesthesia were recruited. Inclusion criteria were American Society of Anesthesiologists (ASA) physical status I–II. Exclusion criteria included (1) history of psychiatric or neurological disorders; (2) alcohol or drug abuse; (3) allergy or intolerance to propofol or benzodiazepines; (4) recent major surgery or trauma (< 14 days); and (5) postmenopausal women or those with severe menstrual disorders.

Anesthesia and monitoring

Prior to the induction of anesthesia, all patients received nasal cannula oxygen (oxygen concentration 100%, oxygen flow rate 5 L/min). Anesthesia was induced with 2.5 mg/kg of propofol and maintained at 2 mg/kg/h propofol via continuous infusion to achieve moderate to deep sedation according to ASA guidelines. Gastrointestinal endoscopy was initiated after confirming the loss of the eyelash reflex. In all patients, a low-dose single injection of remifentanil was administered initially, typically only during anesthesia induction at a dose of 4 μg. Any intraoperative complications (e.g., hypotension, desaturation) were recorded and managed according to standard clinical practice. Furthermore, anesthesiologists administered treatment in accordance with clinical recommendations. In this study, hypotension was defined as a systolic blood pressure below 90 mmHg, and desaturation was defined as SpO₂ below 90%.

Clinical assessments

Euphoria was assessed immediately after recovery using a visual analog scale (VAS, 0–10). Patients with a VAS score ≥ 5 were further evaluated using the morphine-benzedrine group (MBG) subscale of the Addiction Research Center Inventory (ARCI), a validated tool for drug-induced euphoria (Zhao et al. 2023; Zhang and Liu 2013; Liu et al. 1999). The present study has demonstrated that the Cronbach’s alpha for the ARCI scale is 0.86, thus indicating that it exhibits acceptable test–retest reliability (Riba et al. 2001). Sedation levels were assessed with the Observer’s Assessment of Alertness/Sedation Scale (OAA/S), while psychological status was evaluated using the Hospital Anxiety and Depression Scale (HADS) before and after the procedure. Emotional and behavioral observations were conducted in a dedicated post-anesthesia recovery room, where only authorized medical staff were present, ensuring privacy and minimizing external disturbances. All observations were carried out by two senior psychiatric nurses who had received formal training in perioperative psychological assessment and documentation. Their roles were clearly delineated: one nurse continuously monitored patients’ vital signs, while the other focused on documenting behavioral observations using standardized descriptors (e.g., “hand moved to genital area”), thereby avoiding subjective interpretations. If the patient experienced any psychological discomfort, the psychiatric nurses conducting the questionnaire survey could promptly provide more psychological support. Additionally, contact information for professional psychiatrists was provided to all participants for follow-up support if needed.

Network pharmacology analysis

The 2D and 3D structure of propofol was retrieved from PubChem (CID: 4943). Potential molecular targets were predicted using SwissTargetPrediction and DrugBank. Genes associated with female sexual dysfunction (FSD) were obtained from GeneCards and DisGeNET. Overlapping genes between propofol and FSD were identified using Venny 2.1.0.

Protein–protein interaction (PPI) networks were constructed using the STRING 12.0 and visualized in Cytoscape 3.9.1. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed via the DAVID Bioinformatics database, with p < 0.05 and q < 0.05 considered significant.

Molecular docking

The hub targets identified from the PPI network were selected for molecular docking. Protein crystal structures were obtained from the RCSB Protein Data Bank (PDB). PyMOL was used to identify the active binding sites about the original ligand in the potential target protein, eliminate the water molecules, and extract the original ligand, followed by redocking cognate ligands via AutoDock. Further, RMSD analysis was conducted to validate the docking outcomes. The 3D structure of propofol was downloaded from the PubChem database. AutoDock was utilized to achieve molecular docking of propofol with gene targets through the identified docking active sites, and PyMOL was employed for visualization. Propofol’s docking interactions were simulated using AutoDock. LigPlot + was used for analyzing intermolecular interactions.

Statistical analysis

Data were analyzed using SPSS version 21.0 (IBM, Armonk, NY, USA). Continuous variables were presented as mean ± standard deviation or median (IQR) and compared using t-tests or Mann–Whitney U tests, as appropriate. Categorical variables were expressed as n (%) and compared with χ2 tests. A two-tailed p-value < 0.05 was considered statistically significant.

Results

Ethical statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of the First affiliated Hospital of Xiamen University (ID: XMFHIIT-2024SL336). All participants were recruited from the First affiliated Hospital of Xiamen University from July 2024 to December 2024. Written informed consent was obtained from each patient. The psychological assessment was carried out under the guidance of a qualified psychiatrist in our hospital. To avoid bias and possible artificially induced drug dependence, the present research was advised by the Ethics Committee not to discuss the possibility of euphoria with patients in advance. Under the requirements of the local ethics committee, the patients were informed that they were participating in a study of the non-anesthetic effects of propofol, which is scientifically and essentially accurate, but the euphoric effect of propofol was not specifically emphasized in the informed consent form. In this consent, we used alternative language to refer to addiction, such as “emotional changes” rather than using terms that may imply seeking drugs or hint at addiction.

Characteristics of patients

In total, 300 patients were screened for the study. In the male group, four patients were lost to follow-up, five patients refused to answer the question after recovery, and six patients had surgical complications and changed the anesthesia scheme.

All the patients were divided by gender into two groups. There were no differences in age and surgical duration. The demographic data in terms of age, body mass index, and surgery duration were presented in Table 1.

Table 1.

Baseline characteristics of study participants

Gender t p
Male (n = 135) Female (n = 150)
Age 45.37 ± 11.37 43.92 ± 13.67 0.69 0.74
Duration 14.32 ± 3.56 14.98 ± 2.88 2.32 0.56
Height(cm) 172.63 ± 7.44 161.48 ± 5.12 11.56  < 0.001
Weight(kg) 71.39 ± 8.81 62.36 ± 5.62 12.95  < 0.001
BMI 23.67 ± 3.56 22.38 ± 3.47 7.64  < 0.001
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Euphoria, anxiety, and depression of patients

During the awakening phase, atypical behaviors related to self-exploration were observed in a subset of female patients; detailed descriptions are provided in Table S1. During emergence from anesthesia, nine female patients were observed engaging in self-touching behaviors involving the genital and breast areas. In the post-anesthesia care unit (PACU), after full recovery, 42 female and 6 male patients reported visual analog scale (VAS) scores exceeding 5. The incidence of euphoria was significantly higher in females than in males (28.00% vs. 4.44%). The mean ± SD score to VAS was 3.58 ± 2.55 points in the female group, 2.46 ± 1.57 points in the male group. The female group demonstrated a significant enhancement in the VAS score when compared with the male group, with group differences of 1.12 points (95% confidence interval (CI), 0.62 to 1.62; Cohen’s d = 0.52, p < 0.001). The multivariable logistic regression model and sensitivity analyses all demonstrated that gender was the only consistent predictor of euphoria, with females significantly associated with an increased risk of euphoria (adjusted OR = 6.62; 95% CI, 2.46 to 17.81, p < 0.001). The remaining variables demonstrate no significant association with the occurrence of euphoria (Table S2−4). Additionally, the ARCI-MBG score was significantly greater in the female group (11 [9–11]) compared to the male group (9 [7–10]), indicating a sex-related difference (U = 59.50, p = 0.035, r = 0.305) in euphoric responses to propofol (Table S5). Preoperative scores on the Hospital Anxiety and Depression Scale (HADS) did not significantly differ between sexes (Table 2). Intraoperative drug dosages are documented in Table S6.

Table 2.

Assessment of euphoria, sedation, and depression using the Euphoria Rating Scale, OAA/S and HADS

Median [IQR]
Male (n = 135) Female (n = 150) χ2/t p
Euphoria, no. (%) 6 (4.44%) 42 (28.00%) 28.16  < 0.001
OAA/s score 1 [1–1] 1 [1–1] 1.21 0.56
HADS-A score 4 [4–5] 4 [4–5] 3.25 0.64
HADS-B score 2 [2–3] 2 [2–3] 2.68 0.75
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The targets of propofol and its network

The 2D and 3D structures of propofol (PubChem CID 4943) were displayed (Fig. 1a). In the light of the SwissTargetPrediction database, DrugBank database, and a literature, a total of 113 potential targets for propofol were identified. The top 25 target classes were shown via pie chart, including enzyme (20%), ligand-gated ion channel (16%), and family A G group protein–coupled receptor (12%) (Fig. 1b).

Fig. 1.

Fig. 1

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Target genes predicted by the database. a Chemical structure and three-dimensional structure of propofol (PubChem CID 4943). b Categories of top 25 targets for propofol

Identification of female sexual dysfunction screening targets

After executing an all-round search for FSD-related genes in the GeneCards database and DisGeNET database, we identified 1408 genes and 22 genes, respectively. Finally, a set of 1411 unique genes was identified after scrupulous screening and elimination of duplicates.

Analysis of gene topological networks related to female sexual dysfunction and propofol

We constructed the Venny plots of the 113 target genes of propofol and the 1411 FSD-related target genes, which indicated the 37 conjoint genes (Fig. 2a, Table S7). These conjoint genes were imported into STRING 12.0 to generate a PPI network map with Homo species and confidence cutoffs 0.4, comprising 37 nodes and 96 edges, which was input into Cytoscape 3.9.1 (Fig. 2b). Via Centiscape 2.2, we identified and screened out six hub targets from the interaction network based on degree > 5.938, betweenness > 43.188, and closeness > 0.014 (Table S8). A new PPI network map for these hub targets was constructed based on their degree values, with larger nodes and redder colors corresponding to higher degree values (Fig. 2c and d).

Fig. 2.

Fig. 2

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Analysis of gene topological networks related to FSD and propofol. a The Venn diagram of propofol and FSD-related target genes. b PPI network map of target proteins. c The protein–protein network interactions of potential targets. d The protein–protein network interactions in core targets. The number of connected nodes in the network is indicated by the size of the node’s circle, with redder color reflecting a higher connectivity. The color of the edges demonstrates the closeness between nodes, with bluer colors reflecting stronger relationships

GO and KEGG enrichment analysis

To illuminate the functional information and cognate signaling pathways of 37 common target genes, GO and KEGG enrichment analyses were carried out. A total of 236 GO items were obtained, which consisted of 133 biological process (BP) terms, 34 cellular component (CC) terms, and 69 molecular function (MF) terms. According to the p value sorted from smallest to largest, the top ten BPs, CCs, and MFs were visualized, resulting in histograms and a bubble chart (Fig. 3a and b). In terms of BP, they mainly concentrated on cellular response to estrogen stimulus, positive regulation of MAPK cascade, cellular response to peptide hormone stimulus, and other terms. As for CC analysis, their proteins were primarily located in the endosome, perinuclear region of the cytoplasm, plasma membrane, membrane raft, and endosome lumen. In the matter of MF, they largely focused on steroid binding, estrogen response element binding, and other functions. KEGG enrichment analysis identified a total of 44 pathways. Significant enrichment pathways with FDR q-value < 0.05 were presented in Sankey and bubble diagrams (Fig. 3c, Table S9). Further, according to the results of the epidemiological investigation, core targets, and pathway enrichment, the estrogen signaling pathway was highlighted, and the schematic diagram of propofol in the treatment of FSD by targeting the estrogen signaling pathway was shown in Fig. 4b.

Fig. 3.

Fig. 3

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GO and KEGG enrichment analysis of 37 target genes. a The top 10 terms enriched entries for each GO category (BP, CC, and MF). b The size of each bubble corresponded to gene expressions in a particular pathway. c The KEGG pathway for core targets Sankey and bubble diagrams

Fig. 4.

Fig. 4

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Drug-target-pathway-disease network diagrams and distribution of core targets in the main pathways. a Drug-target-pathway-disease network diagram for the effect of propofol against FSD. b Diagrams of the estrogen signaling pathway, highlighting the target that is common to both propofol and FSD, represented in red color

Propofol against female sexual dysfunction network analysis

The target network diagram of propofol against female sexual dysfunction was constructed by Cytoscape to form a “drug-target-pathway-disease” network diagram (Fig. 4a). The green ellipse represents propofol, the yellow diamond represents the target genes, the orange hexagon represents the pathways, and the blue octagon represents FSD. The diagram provides information on the target genes, the pathway, and the degree of propofol against female sexual dysfunction.

Molecular docking analysis

The hub targets in the PPI network were selected for molecular docking with propofol, namely ESR1, EGFR, APP, NR3C1, MDM2, and MAOB. The results demonstrated that the RMSD was less than 2.0 Å, and all binding energies were lower than − 5.0 kcal/mol (Table 3), indicating propofol displayed effective and stable binding to all genes. Hydrogen bonding suggests stable binding of propofol to hub targets (Fig. 5). Meanwhile, the best-docked conformation is indicated by the lowest binding energy between the ligand and receptor (it has to be a negative value). The lower the binding energy, the stronger binding becomes, manifesting a greater potential therapeutic target.

Table 3.

Results of molecular docking validation, including redocking of cognate ligands and RMSD analysis

Target PDB ID Binding energy (kcal/mol) Ligand Active binding site (X, Y, Z) RMSD(Å)
ESR1 2QXS  − 6.6 RAL (17.192, −17.319, 22.870) 1.06
EGFR 1M17  − 6.0 AQ4 (21.857, 0.260, 52.761) 0.51
APP 3KTM  − 5.9 BU4 (16.216, 24.124, −33.855) 0.69
NR3C1 4P6X  − 6.3 HCY (25.630, 107.853, −31.253) 0.81
MDM2 1RV1  − 5.5 IMZ (10.459, 7.405, 14.256) 0.08
MAOB 6FW0  − 7.0 E92 (50.915, 155.605, 28.451) 0.32
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Fig. 5.

Fig. 5

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3D binding conformations and 2D interaction diagrams of propofol with FSD-related hub targets. a ESR1; b EGFR; c APP; d NR3C1; e MDM2; f MAOB. Binding energies are indicated below each docking panel

Discussion

It is estimated that up to 40% of women experience female sexual dysfunction (FSD), with prevalence in Asia likely underestimated due to cultural barriers. FSD exerts a profound psychological and interpersonal impact, yet it remains under-researched and undertreated. Sexual arousal disorders and sexual desire disorders are among the most common subtypes, but their mechanisms in peri-anesthetic contexts are largely unknown. Recent evidence suggests that anesthetics may influence mood regulation (Reinert and Parmentier 2021; Zhu et al. 2023), providing a rationale for investigating their role in sexual function.

In this study, we observed that women had a markedly higher incidence of propofol-induced euphoria than men, with some patients displaying behaviors suggestive of enhanced sexual euphoria. Significantly, all behaviors were spontaneously initiated by the patients, with researchers engaging solely in passive observation without any induction or interference (all data were fully anonymized and cannot be traced back to any individual). This phenomenon is reported purely for scientific descriptive purposes to reveal the unique effects propofol may produce. It is well established that propofol exerts its sedative effects through GABA-A receptors (Philip AB et al. 2025). However, extant mechanisms are inadequate in explaining the euphoric effects it engenders, nor can they account for the gender differences in euphoria. The differences of gender on the induction of euphoria by propofol may be subject to a multitude of factors. (1) Gender pharmacokinetic differences: variations in propofol distribution volume, body fat content, and metabolic rate between males and females may partially contribute to the observed differences. (2) Hormonal cycle phase: fluctuations in endogenous hormones caused by the menstrual cycle or exogenous hormones (e.g., contraceptives) may induce observed discrepancies. (3) Cultural reporting bias: differences in willingness and accuracy of reporting sensitive issues like sexual function may exist across cultural contexts. However, the abovementioned factors do not provide a comprehensive explanation for this phenomenon. Therefore, the study raised the possibility that propofol transiently modulates affective states through estrogen- and progesterone-related pathways involved in reward and sexual function.

Network pharmacology identified 113 potential targets for propofol, and 1411 genes associated with FSD. Intersection analysis revealed 37 overlapping genes, which clustered in pathways related to estrogen signaling, steroid binding, nitric oxide synthase activity, and cGMP-dependent cascades. Molecular docking further demonstrated strong binding affinities of propofol with ESR1, EGFR, APP, NR3C1, MDM2, and MAOB, implicating these targets in both mood regulation and sexual response.

Estrogen receptor signaling, including both ERα/ERβ genomic and GPER non-genomic pathways, plays a critical role in neural networks regulating sexual desire and arousal (Gui et al. 2025; Micevych and Kelly 2012; Santoro et al. 2016). Epidermal growth factor receptor (EGFR), which interacts with estrogen pathways in diverse contexts such as cancer and cognition (Aguirre et al. 2010; Liang et al. 2023), may also contribute to propofol’s effects, although its influence on rapid GPER-mediated signaling requires further study. Amyloid beta precursor protein (APP), classically linked to Alzheimer’s disease, has been associated with sexual behavior in animal models (Gadomsky et al. 2020; Park et al. 2010), suggesting a potential but underexplored role in reproductive neurobiology.

Nuclear receptor subfamily 3 group C member 1 (NR3C1), encoding the glucocorticoid receptor, is central to stress regulation (Bereshchenko et al. 2018), while monoamine oxidase B (MAOB) modulates serotonin metabolism, both of which are closely linked to anhedonia and sexual dysfunction (Atmaca 2020; Croft 2017; Giatti et al. 2018; Spies et al. 2020; Watkeys et al. 2018; Xie et al. 2025). Murine double minute clone 2 (MDM2) is a pivotal regulator of the p53 gene. One study has indicated an association between MDM2 and drug addiction. Specifically, the MDM2 gene has been observed to be upregulated in the brain following the administration of addictive substances (Jiang et al. 2003). Furthermore, ultraviolet irradiation has been observed to elevate estrogen levels in animals and enhance sexual behavior via the p53 gene (Parikh R et al. 2021). Propofol’s affinity for these targets highlights its potential influence on stress- and mood-related mechanisms underlying FSD.

Clinically, these findings suggest that propofol-induced euphoria may not simply be an incidental anesthetic effect, but rather a reproducible pharmacological phenomenon with potential therapeutic relevance. Current options for FSD, especially HSDD, remain limited and often ineffective. Our results provide preliminary evidence that propofol, or structurally related compounds, could be explored as novel candidates for managing anhedonia in women with FSD, which requires further experimental verification.

This study has some limitations. Firstly, the study was conducted at a single center with a relatively small sample size, which may limit the generalizability of the findings to broader populations. Secondly, due to the observational nature of the study, neither patients nor investigators were blinded, and no randomization was performed. This may have introduced observer bias when assessing subjective outcomes such as euphoria. The utilization of subjective tools for the evaluation of euphoria may be vulnerable to recall bias and social desirability bias. Thirdly, the study did not collect information regarding menstrual phase, the use of hormonal contraceptives, and hormone therapy. In future prospective studies, we plan to systematically capture these variables using standardized questionnaires and/or serum hormone level testing. Furthermore, the rigid docking approach currently employed fails to account for protein conformational flexibility and the mediating role of key water molecules. Subsequent studies will employ more advanced methodologies, including adding a consensus/secondary scoring, evaluating candidate compound efficacy through enzyme activity inhibition assays, validating reporter genes (e.g., estrogen receptor reporter genes) in cellular models, and conducting target binding validation using chemical epigenomic target screening (CETSA) and molecular spontaneity targeting (MST) technologies. Finally, it is possible that cultural factors may have influenced the reporting of sexual symptoms in this Chinese cohort, potentially limiting the direct generalizability of results to cultures with distinct sexual attitudes and expressions.

In conclusion, propofol may modulate estrogen receptor–related and monoamine pathways, which may lead to transient euphoria in women and reveal novel insights into mechanisms underlying female sexual dysfunction. Further multicenter and mechanistic studies are warranted to confirm these findings and explore their therapeutic implications.

Supplementary Information

Below is the link to the electronic supplementary material.

ESM 1 (57.1KB, docx)

(DOCX 57.0 KB)

Acknowledgements

The authors express gratitude to all participants.

Abbreviations

FSD

Female sexual dysfunction

HSDD

Hypoactive sexual desire disorder

ESR1

Estrogen receptor 1

EGFR

Epidermal growth factor receptor

APP

Amyloid beta precursor protein

NR3C1

Nuclear receptor subfamily 3 group C member 1

MAOB

Monoamine oxidase B

ASA

American Society of Anesthesiologists

VAS

Visual analog scale

ARCI-MBG

Addiction Research Center Inventory Morphine–Benzedrine Group

OAA/S

Observer’s Assessment of Alertness/Sedation Scale

HADS

Hospital Anxiety and Depression Scale

PPI

Protein–protein interaction

GO

Gene Ontology

KEGG

Kyoto Encyclopedia of Genes and Genomes

RMSD

Root mean square deviation

BP

Biological process

CC

Cellular component

MF

Molecular function

Author contribution

L. Wang: Conceptualization, methodology, software, validation, formal analysis, investigation, data curation, visualization, writing—original draft preparation, writing—review and editing. Z. Liao: Conceptualization, methodology, software, validation, formal analysis, investigation, data curation, visualization, writing—original draft preparation, writing—review and editing. G. Qiu: Conceptualization, methodology, software, validation, formal analysis, investigation, data curation, visualization. B. Yang: supervision, writing—original draft preparation, writing—review and editing. The authors declare that all data were generated in-house and that no paper mill was used.

Funding

This work was supported by The Natural Science Foundation of Fujian Province (No. 2022J011369), Fujian Research and Training Grants for Young and Middle-aged Leaders in Healthcare (to Bin Yang).

Data availability

All source data for this work (or generated in this study) are available upon reasonable request.

Declarations

Ethics approval

This study was conducted in accordance with the Declaration of Helsinki and approved by the Ethics Committee of the First Affiliated Hospital of Xiamen University (ID: XMFHIIT-2024SL336).

Consent to participate

Informed consent was obtained from all individual participants included in the study.

Consent for publication

All authors agree to the publication of the manuscript.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Linhong Wang and Zhongli Liao contributed equally to this work.

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