To ensure comprehensive coverage of relevant literature, a systematic search was conducted across three academic databases and one altmetrics platform. The selected academic databases—Web of Science Core Collection (WoSCC), Scopus, and PubMed Central (PMC)—were chosen for their academic rigor and extensive coverage of the biomedical literature. Altmetric data, collected via Altmetric Explorer (www.altmetric.com), include the Altmetric Attention Score (AAS) and mentions across news outlets, social media platforms, and policy documents.

The search strategy combined keywords related to “P2Y receptor” and “cardiovascular disease” and used wildcards and truncators to cover all variants, with P2Y-related terms: “P2Y,” “Purinergic P2Y Receptors,” “P2Y Purinoceptor” and cardiovascular disease related terms: “cardi” (covering “cardiology,” “cardiovascular,” “cardiac,” etc.) as topics. The search was limited to English articles and reviews published between 2005 and 2025 (up to 7 July 2025), and a total of 10,483 articles were retrieved. Two independent investigators (Mengyu Yang and Xuanrui Chen) screened titles and abstracts to exclude irrelevant studies (e.g., non-cardiovascular, non-human/non-clinical studies) and duplicate articles, and differences were resolved by consensus or consultation with third-party investigators (Jingchun Zeng), resulting in 2,591 articles included. This data is used to analyze and visualize authors, institutions, countries, journals, co-cited references, and keywords. Figure 1 illustrates the search and screening process.

Three primary tools were employed for bibliometric analysis. CiteSpace (version 6.4.1) (Chen, 2020) was used to construct author-institution collaboration networks and keyword co-occurrence maps, and to detect citation bursts for identifying emerging research frontiers. VOSviewer (version 1.6.20) (van Eck and Waltman, 2010) was utilized to visualize co-citation networks, national collaboration networks, and journal relationships. In these visualizations, node size corresponds to the number of publications, and connection thickness indicates the strength of collaboration. The Bibliometrix R package (Aria and Cuccurullo, 2017) was applied to quantify annual publication trends, journal distributions, and citation metrics, including total citations and the h-index.

Data from Altmetric Explorer (www.altmetric.com) were used to obtain the Altmetric Attention Score (AAS) for each publication and to identify highly mentioned articles. We extracted AAS data and mention counts from various sources, including news outlets (e.g., The New York Times), social media platforms (e.g., Twitter/X), and policy documents to assess the broader societal impact of the research. The Spearman correlation coefficient was calculated to analyze relationships, and a p-value of <0.05 was considered statistically significant for assessing the validity of the observed societal impact.

The trend of annual and cumulative publications provides a key empirical basis for evaluating the current development of the field and predicting its future trend. As shown in Figure 2, the study of P2Y receptors in the CVDs has experienced three distinct growth phases between 2005 and 2025. The initial period, from 2005 to 2010, was the embryonic stage, marked by an explosive growth in annual publications, which surged from 12 to 248. This represented an impressive average annual growth rate of 60% and a 20-fold increase in cumulative publications, signifying a critical point of expansion that laid the groundwork for future advancements. The second phase, from 2011 to 2019, was one of steady expansion. During this time, the number of annual papers fluctuated but generally stabilized between 100 and 200, with the cumulative total surpassing 1,500. The research focus shifted from basic mechanisms to clinical translation. While the total volume expanded by 4.2 times, the average annual growth rate moderated to 22%, and the ratio of new papers to the existing stock decreased from 90% to 13%, indicating a shift from a rapid growth phase to stable development. The third and current phase, from 2020 to 2025, represents the mature period. The annual publication volume has been maintained at around 200 articles, with a slower annual growth rate of 11.6%. New research priorities have emerged, focusing on precision medicine and drug resistance mechanisms. Over this decade, the cumulative number of published papers increased by 148%, with a compound annual growth rate of approximately 10.5%. Although the figures for 2025 are not yet complete, strong growth is expected to continue. The continuous increase in both cumulative and annual publications powerfully demonstrates the growing academic vitality of P2Y receptor research in the CVDs field, attracting increasing attention from the scientific community.

VOSviewer 1.6.20 and CiteSpace 6.4.1 software were used to analyze the author collaboration network and institutional research pattern of P2Y receptors in the CVDs research field, including data from 12,292 authors and 4,653 institutions, revealing the core academic strength and global collaboration characteristics of this field.

The global research landscape comprises 68 countries and regions, organized within a highly centralized collaboration network (Supplementary Figure 4). The United States, with 941 articles, acts as the central hub for international cooperation. China (367 articles) and Italy (333 articles) serve as critical regional sub-centers within the Asian and European networks, respectively (Supplementary Table 2). The strategic partnership between China and the United States exemplifies the efficacy of such transnational collaboration. By integrating large-scale clinical cohorts from China with experimental design protocols from the United States, a joint study elucidated the molecular mechanisms of platelet activation in diabetic patients (Hu et al., 2017), Published in Circulation, this work demonstrates how cross-border synergy can accelerate the translation from basic target discovery to therapeutic optimization.

This study employed VOSviewer to analyze the journal sources of published literature and co-cited references, thereby identifying the core academic platforms and influence of P2Y research within the field of CVD_S.

Keyword co-occurrence and burst detection analyses delineated the core themes, evolving hotspots, and emerging trends in P2Y receptor research related to CVDs. The keyword co-occurrence network generated by CiteSpace comprises 395 nodes, with node size proportional to frequency of occurrence. Nodes with a purple outer ring denote high betweenness centrality, while those highlighted in red represent keywords with citation bursts (Supplementary Figure 7).

In this study, we employed CiteSpace to perform a co-citation analysis of 2,637 included references, tracing the evolution of landmark research and knowledge pathways related to P2Y receptors within the CVD_S research field. The resulting co-citation network comprises 690 nodes, 1,278 links, and five clusters (Supplementary Figure 11; modularity Q = 0.7476, mean silhouette S = 0.8915), reflecting a well-defined clustering structure and high thematic coherence.

To comprehensively capture the diversity of knowledge on P2Y in cardiovascular disease (CVD) and to counterbalance the predominance of clinical studies among the most-cited works, we implemented a tiered screening strategy. This process selected the ten most representative, highly cited articles (each with ≥160 citations, Table 1) from distinct research categories, comprising four clinical studies, four basic or translational studies, one guideline, and one narrative review. This selection essentially spans the complete knowledge chain from receptor biology and pharmacogenomics to therapeutic decisions and normative documents. We also analyzed the top ten articles ranked by Altmetric Attention Score (AAS) Supplementary Table 5. The results show that over half of the high-AAS articles were published between 2019 and 2023, primarily addressing the optimization of P2Y₁₂ receptor inhibitor use in acute coronary syndrome and other high-risk contexts. Notably, a study led by Lars Wallentin appeared on both the high-citation and high-AAS lists, achieving an AAS of 658 and thereby demonstrating a dual performance of high academic impact and broad societal attention.

Spearman correlation analysis elucidated the relationships between the AAS and its constituent attention dimensions. The strongest correlations were between AAS and mentions on platform X (r = 0.5957, p < 0.001) and news mentions (r = 0.5441, p < 0.001), indicating that social media and news coverage were the primary drivers of the Altmetric score in this sample. Moderate correlations existed with clinical guideline citations (r = 0.3984, p < 0.001), Dimensions citations (r = 0.3743, p < 0.001), and Mendeley readership (r = 0.3705, p < 0.001). Positive correlations of moderate strength were also observed for Facebook and blog mentions (r ≈ 0.35, all p < 0.001). In contrast, policy document mentions, patent citations, Wikipedia mentions, and F1000 mentions showed weaker correlations with AAS. Correlations between AAS and Weibo mentions or peer-review mentions were negligible, while Reddit mentions showed no significant correlation. This pattern indicates that for P2Y-related cardiovascular research, the Altmetric signal is driven primarily by English-language social and news media, which subsequently influences more traditional evaluation systems through guideline and academic citations.

Several potential confounding factors must be considered when interpreting the only moderate correlation between AAS and citation-based metrics, though they are only briefly highlighted here. First, publication eras differ; many highly cited basic science and pharmacogenomic studies were published before social media was prevalent or Altmetric coverage was comprehensive, making their online attention unlikely to match their long-term citation accumulation. Second, journal influence and its dissemination resources can affect AAS, as high-impact journals often amplify a study’s online visibility through press releases. Third, Altmetric primarily captures the English-language digital ecosystem, with limited coverage of non-English regions. These factors collectively complicate the establishment of a simple linear relationship between AAS and traditional citations.

In summary, thematic differences between highly cited and high-AAS literature remain evident. High-AAS literature concentrates more on issues with direct clinical or public health implications, such as comparisons between P2Y₁₂ receptor inhibitors, antiplatelet regimen optimization in acute coronary syndrome, and safety signals regarding antithrombotic drug interactions during the COVID-19 pandemic. These topics are more prone to trigger media coverage and social media discussion. Highly cited literature, conversely, focuses more on P2Y receptor biology and signal transduction, receptor structure elucidation, pharmacogenomic evidence for drug response, and evaluations of long-term antithrombotic strategies. The former reflects translatable topics with high dissemination potential, while the latter constitutes the structural foundation of domain knowledge. Together, they delineate the distinct evolutionary trajectories of P2Y receptor-related research along the dual pathways of academic citation and societal discussion.

Cross-interpretation of keyword co-occurrence clusters, burst dynamics, and co-citation clusters indicates that thematic differentiation in P2Y-related cardiovascular research is driven primarily by clinical decision-making challenges. In the co-occurrence network, high-frequency terms such as clopidogrel, PCI, and myocardial infarction have long occupied a central position. Concurrently, terms with high-degree connectivity, including bleeding, drug dose, and DAPT, have risen in prominence. This pattern suggests a shift in research focus from verifying efficacy and feasibility toward the refined optimization of administration timing, dosage selection, and population stratification.

LSI clustering and timeline analyses further delineate this transition through three progressive themes: (1) procedural optimization of P2Y₁₂ inhibitor timing and switching, which addresses practical challenges like oral loading during cangrelor bridging and avoids “efficacy gaps” in urgent or perioperative scenarios; (2) response variability and stratified therapy, exemplified by CYP2C19 testing and high on-treatment platelet reactivity (HTPR); and (3) strategic rebalancing focused on bleeding risk control and duration optimization within dual antiplatelet therapy (DAPT). Temporally, DAPT demonstrated the strongest citation burst (strength: 46.85) from 2019 to 2025, marking it as a primary recent growth area. The co-citation network corroborates this by revealing a structural shift in the field’s knowledge base from “establishing consensus through landmark trials” toward “regimen adjustment under safety constraints.” Specifically, the PLATO trial, the node with the highest burst strength (62.64), corresponds to the transition from clopidogrel-based regimens to more potent P2Y₁₂ inhibition with ticagrelor. Subsequently, high-burst studies focusing on “de-escalation” and “monotherapy” have formed a bridging theme that links the evidence chains for “efficacy enhancement” and “bleeding control,” thereby reflecting ongoing debate on risk-stratification-guided antithrombotic strategies.

Furthermore, the “short-term DAPT—de-escalation/monotherapy—stratified decision-making” axis identified through this cross-interpretation is not an isolated network phenomenon but corresponds directly to recent clinical research and evidence updates. The SHARE randomized trial showed that switching from DAPT to P2Y₁₂ inhibitor monotherapy 3 months after PCI was non-inferior to 12-month DAPT with respect to NACE, supporting the viability of a strategy involving shortened combination therapy followed by P2Y₁₂ inhibitor monotherapy (Min et al., 2024). Systematic reviews and meta-analyses in ACS populations further demonstrate that P2Y₁₂ inhibitor monotherapy after short-term DAPT significantly lowers bleeding risk without increasing ischemic events, while also hinting at potential stratified benefits between different agents, such as ticagrelor versus clopidogrel (Galli et al., 2024).

In individualized medication, CYP2C19 genotyping—especially for loss-of-function [LOF] carriers—and high on-treatment platelet reactivity (HTPR) assessments guide the escalation or de-escalation of P2Y₁₂ inhibitor therapy. For patients carrying LOF alleles or exhibiting HTPR alongside high ischemic risk, switching from clopidogrel to ticagrelor or prasugrel is preferred to mitigate ischemic events. Conversely, for patients with lower ischemic but higher bleeding risk, de-escalation from potent P2Y₁₂ inhibitors to clopidogrel or shortening dual antiplatelet therapy (DAPT) duration after the acute phase is considered, thereby operationalizing the “CYP2C19–HTPR” framework into stratified treatment pathways (van den Broek et al., 2024). A 2025 individual participant data meta-analysis in the BMJ further compared P2Y₁₂ inhibitor monotherapy with aspirin monotherapy as maintenance therapy after DAPT discontinuation, reinforcing the re-evaluation of long-term strategies as a current focus (Giacoppo et al., 2025).

The convergent trajectory from co-occurrence, burst detection, and co-citation analyses indicates that research hotspots are increasingly centered on actionable clinical decision points, such as duration selection, medication bridging, and stratified decision-making. These themes appear in bibliometric maps as highly connected terms and high-burst keywords, corresponding to points of divergence frequently debated in recent trials and reviews. This alignment offers a reference for more refined subsequent evidence synthesis and clinical study design.

The imbalance between inflammation and immune response constitutes a central mechanism in the development of CVDs (Wang Z. et al., 2025; Gupta et al., 2023). P2Y receptors detect extracellular nucleotides such as ATP and ADP, thereby contributing to immune cell activation and inflammatory cascades (Le Duc D et al., 2017; Thomas and Storey, 2015b),although their functions are highly subtype-specific and context-dependent (Klaver and Thurnher, 2021).

The mechanisms of pro-inflammatory subtypes are well-established: P2Y₁, P2Y₂, P2Y₆, and P2Y₁₄ primarily promote inflammation. The P2Y₁ receptor enhances TNFα-induced vascular inflammation by upregulating leukocyte adhesion molecule expression in endothelial cells (Zerr et al., 2011). Activation of the P2Y₆ receptor stimulates the release of pro-inflammatory factors such as IL-6 and TNF-α via the macrophage NLRP3 inflammasome and accelerates atherosclerosis (Collado and Zhou, 2025); The P2Y₁₄ receptor is activated by UDP-G and amplifies neutrophil infiltration through chemokine-mediated recruitment (Zhang et al., 2024). These subtypes collectively drive disease progression through a cascading process involving “injury signal detection–inflammatory mediator release–pathological amplification”.

The function of anti-inflammatory and regulatory subtypes is reflected in their maintenance of immune homeostasis; P2Y₁₁ receptors interact with the IL-1R pathway to promote macrophage M2 polarization and participate in tissue repair (Klaver and Thurnher, 2023). P2Y₁₂ exhibits a particularly typical dual role, as its activation induces platelets to release P-selectin, thereby exacerbating inflammation (Lee et al., 2023).Antagonists such as ticagrelor reduce inflammatory responses by inhibiting platelet–leukocyte interactions (Mansour et al., 2020), which depend bidirectionally on the pathological stage and cellular microenvironment (Xiao et al., 2024).

A key bottleneck in current research is the lack of clinically available, highly selective modulators for most receptor subtypes, and differences in expression between animal models and humans limit the extrapolation of results. Future studies should integrate single-cell sequencing and spatial transcriptomic technologies to analyze the spatiotemporal expression patterns of P2Y receptors within specific cellular subsets, thereby providing a foundation for precise anti-inflammatory interventions.

Throughout myocardial ischemia/reperfusion injury and post-infarction repair, P2Y receptors function as a signaling hub coordinating the entire “injury–repair–regeneration” continuum by mediating cross-talk among cardiomyocytes, immune cells, and endothelial cells (Tobin et al., 2020; Djerada et al., 2017). In myocardial protection, receptor subtypes including P2Y₁₂, P2Y₂, P2Y₄, and P2Y₁₄ play pivotal roles. The P2Y₁₂ receptor has attracted particular research interest due to its central position within platelet–immune–vascular networks (Puthanveedu et al., 2025). As a key mediator of ADP-induced platelet aggregation, P2Y₁₂ antagonists such as clopidogrel reduce thrombosis and exert cardioprotective effects in myocardial infarction and ischemia/reperfusion injury (Zhang et al., 2017). P2Y₁₂ expression in vascular smooth muscle and endothelial cells also modulates inflammatory mediators such as MCP-1, thereby contributing to vascular inflammation (Satonaka et al., 2015). Although direct evidence for a role in myocardial regeneration is lacking, the synergistic anti-inflammatory and antithrombotic effects of P2Y₁₂ inhibition indirectly support cardiac repair, particularly given the influence of inflammation on regenerative capacity (Li et al., 2023).

The P2Y₁₄ receptor recognizes UDP-glucose and induces neutrophil polarization toward a proinflammatory (N1) phenotype; its antagonist PPTN promotes a shift to the anti-inflammatory (N2) phenotype, thereby attenuating myocardial inflammation (Zhang et al., 2024). indicating its potential cardioprotective value. As a UTP-activated receptor subtype, P2Y₄ demonstrates cardioprotective potential in myocardial ischemia/reperfusion injury (I/R): its activation is closely linked to intracellular Ca²⁺ dynamics, influences tissue repair via endothelial cell function and cardiac progenitor cell activity (Djerada et al., 2017), and may contribute to post-ischemic repair by regulating cell proliferation, migration, and anti-apoptotic mechanisms (Rafehi et al., 2017).

The role of P2Y₂ receptors in myocardial protection and regeneration has been experimentally validated and holds direct therapeutic promise. Studies using in vitro models, mouse experiments, and isolated heart perfusion demonstrate that both UTP and the P2Y₂R agonist MRS 2768 significantly reduce myocardial infarct size following I/R injury by activating P2Y₂ receptors, improving cardiac function in a dose-dependent manner (Li et al., 2016; Cohen et al., 2011). These findings underscore its critical role in preserving cardiomyocyte integrity and function and countering ischemic injury (Khalafalla et al., 2017). Furthermore, P2Y₂ receptors act as signaling nodes that support cardiomyocyte survival, endothelial cell function, and cardiac progenitor activation through regulation of intracellular Ca²⁺ concentrations and ERK1/2 pathways (Chang et al., 2008; Muscella et al., 2003; Weisman et al., 2001). However, P2Y₂ also mediates fibrogenic responses in fibroblasts, suggesting a dual role in regenerative regulation (Braun et al., 2010), that warrants further refinement of targeting strategies.

In summary, P2Y receptors do not operate as isolated pathway components in myocardial protection and regeneration, but rather function as signaling hubs integrating multiple cell types. Their actions exhibit marked subtype specificity, cell-type dependency, and stage-dependent variation across pathology, forming a coordinated signaling network throughout the process of “damage–inflammation–repair–regeneration.” Future studies should prioritize delineating the spatiotemporal expression patterns of P2Y receptors across distinct cellular subsets to enable the development of precise interventional strategies.

Our co-citation analysis identified specific “structural turning points” that have reshaped clinical practice. The high burst strength of landmark studies, such as the PLATO trial, quantitatively marks the transition from clopidogrel to ticagrelor. This shift established P2Y12 antagonists as a key therapeutic strategy for the secondary prevention of atherosclerotic cardiovascular events (Angiolillo et al., 2017). The subsequent rise of “genotype-guided therapy” clusters (Cluster #4) reflects the integration of CYP2C19 testing into precision medicine (Al-Abcha et al., 2022). A current “de-escalation” shift is exemplified by the TROPICAL-ACS study, which demonstrated that a guided step-down strategy reduces bleeding events without elevating ischemic risk (Sibbing et al., 2017). A contemporary “de-escalation” shift is now underway, evidenced by the high centrality of studies focusing on bleeding risk reduction. Recent evidence from the TACSI study (Jeppsson et al., 2025). However, critically reminds us that intensified strategies are not universally applicable. This aligns with our bibliometric finding that “bleeding risk” and “individualization” have become dominant high-frequency keywords, driving the transition from “the more, the better” to “less is more” in antithrombotic strategy.

Significant progress has also been made in elucidating the X-ray crystal structures of small molecule ligands bound to both P2Y₁ and P2Y₁₂ receptors, while a cryo-electron microscopy structure of the P2Y₂–Gq protein complex has further revealed the molecular basis of ligand recognition and signal transduction (Lan et al., 2025). Fluorescent imaging probes, high-affinity radioligands, and high-throughput screening methods have substantially enhanced the resolution of P2Y receptor activation and antagonist binding kinetics (Stéen et al., 2025). These structural and technological advances provide a foundation for the precise modulation and targeted drug design of P2Y₁, P2Y₂, P2Y₆, and other subtypes, facilitating the development of more selective and safer P2Y receptor-based therapeutics with expanded potential in cardiovascular disease (Puthanveedu et al., 2025). As structural analysis and screening technologies continue to advance, novel P2Y receptor modulators may integrate genotyping, functional phenotyping, and disease stratification strategies, thereby shifting the paradigm from single-target inhibition toward precise targeting and individualized intervention, and offering more tailored treatment options for diverse cardiovascular conditions.

In recent years, research on P2Y receptors within the field of CVDs has exhibited a notable trend toward interdisciplinary integration, centered on incorporating nano-delivery systems, multi-omics analysis, artificial intelligence modeling, and real-time monitoring into drug development and functional regulation. Advances in materials and biotechnology have enabled Guo et al. (2024) to develop P2Y₁₂-overexpressing cell membrane-coated nanoparticles that reverse the effects of antiplatelet drugs in vivo; Qin et al. (2025) outlined a strategy using micro-nano motors to assist targeted delivery of P2Y₆ antagonists to atherosclerotic plaques, offering a novel approach for precise drug transport. In drug screening and mechanistic studies, Han et al. (2023) and Zhao et al. (2024) performed virtual screening based on domain rigidity and receptor scaffold design for P2Y₁₄ and P2Y₆, respectively, facilitating the identification of high-affinity compounds. Multi-omics and sensing technologies further support the elucidation of functional mechanisms and individualized monitoring: Collado and Zhou (2025) uncovered signaling pathways mediated by P2Y₆ that promote foam cell formation, providing systematic validation for target identification. Dambruoso et al. (2024) employed thromboelastography (TEG) to monitor intraoperative bleeding risk associated with P2Y₁₂ inhibitors, while Ahmad et al. (2025) developed a wearable sensor for real-time assessment of platelet activation. Artificial intelligence models also enhance personalized treatment approaches: Ortega-Paz et al. (2024) predict efficacy based on eGFR, Lin et al. (2025) integrated genetic data and coagulation parameters to construct a dose optimization system. Moreover, multi-scale modeling has revealed synergistic effects of P2Y₁/P2Y₁₂ signaling in thrombus stability (Bouchnita and Volpert, 2024; Patel et al., 2025), and implicated P2Y receptors in inflammation-thrombosis crosstalk (Seung et al., 2022) and vascular homeostasis regulation (Chen et al., 2024; Daghbouche-Rubio et al., 2024), opening new avenues for therapeutic expansion. Current challenges include limited subtype selectivity (Han et al., 2023) and interference from receptor heterodimerization (Puthanveedu et al., 2025). Future breakthroughs will require deeper integration of emerging technologies with P2Y receptor-specific regulatory strategies to achieve dynamic, stratified, and controllable intervention of P2Y signaling across disease states.

Based on the joint analysis of Altmetric and citation metrics, this study reveals a significant disparity between the academic community and the general public in their attention to the same body of knowledge within P2Y receptor-related cardiovascular research. As shown in Supplementary Figure 14, the Altmetric Attention Score (AAS) correlates more strongly with activity on platform X and news coverage than with traditional citation metrics, demonstrating only a moderate positive correlation with citation counts and Mendeley readership. This pattern indicates that Altmetric primarily captures online attention centered on English-language social media and news outlets, rather than the academic impact traditionally reflected by cumulative citations. The observed “correlated but non-overlapping” relationship does not signify the superiority of one evaluation system over another but results from several intertwined structural factors. First, publication date directly influences the misalignment between academic and societal attention. Many highly cited foundational and translational studies were published before the rise of social media and systematic Altmetric data collection. While these works hold significant positions in traditional citation databases, they correspondingly lack societal resonance in terms of AAS. Conversely, more recent clinical and translational studies often benefit from multi-channel dissemination, such as journal press releases and official social media promotions, allowing them to achieve high AAS rapidly despite being in early stages of citation accumulation. Second, the dissemination capacity of the publishing journal itself is a critical variable. High-impact cardiovascular journals typically employ professional media teams and maintain active social media channels to proactively promote papers with clinical or public health significance. Consequently, studies of comparable academic merit tend to achieve greater Altmetric prominence when published in such venues. In contrast, studies published in highly specialized or lower-impact journals may be undervalued in Altmetric assessments despite reporting groundbreaking findings in areas like receptor mechanisms or pharmacogenomics, due to their limited dissemination resources. Furthermore, an inherent dissemination bias within the Altmetric system itself cannot be overlooked. Its scoring relies heavily on activity from English-language social platforms and news outlets, while discussions from non-English regions or specific online communities are less represented, thereby concentrating “global attention” along linguistic and geographical lines and amplifying evaluation imbalances.

After identifying these confounding factors, comparing high-AAS literature with highly cited literature provides a more nuanced understanding of the differing focus between academic and societal attention. High-AAS literature predominantly addresses topics with direct implications for clinical decision-making or public health, such as studies on different P2Y₁₂ receptor inhibitors, antiplatelet strategies in acute coronary syndromes, and drug interactions in the context of emerging infectious diseases. This type of research is more likely to be covered by news media and reinterpreted by clinicians, patients, and policy groups on social media, thus holding an inherent advantage within the dimensions constituting the AAS. In contrast, highly cited literature more frequently addresses fundamental and methodological issues, such as the crystal structure and signal transduction networks of P2Y receptors, long-term follow-up evidence on the impact of genetic polymorphisms on drug response, and systematic evaluations of long-term antithrombotic strategies. Such work resists translation into public-facing communication narratives in the short term, resulting in relatively limited online traction. Over a longer timescale, however, it is continuously cited and expanded upon by subsequent research, forming the deep skeleton of the field’s knowledge system. Therefore, the “academic-societal attention misalignment” observed here primarily reflects differences in evaluation dimensions and temporal scales: AAS is more sensitive to recent, clinically relevant research that is easily disseminated, whereas traditional citations accumulate persistently around studies with enduring conceptual and methodological contributions. In assessing the impact of P2Y receptor-related cardiovascular research, juxtaposing Altmetric metrics with citation-based metrics—rather than substituting one for the other—serves a dual purpose. This approach helps identify which studies are currently generating spillover effects on clinical practice and policy, while also suggesting that researchers should consider designing differentiated communication strategies for different audiences. Only by fully accounting for structural factors such as publication age, journal influence, and social media biases can the relationship between the Altmetric Attention Score and citation metrics be accurately understood and effectively utilized to guide future research and knowledge translation in the P2Y field.

This study has several inherent limitations. First, our analysis was restricted to English-language publications indexed in major bibliographic databases. This selection criterion introduces a coverage bias, as mainstream indexing systems prioritize internationally oriented journals. Consequently, significant research outputs—particularly those focusing on community-based interventions and patient-centered outcomes—may be systematically overlooked.This exclusion risks marginalizing unique clinical evidence rooted in specific regional practices, which could lead to a biased assessment of the field’s structural evolution (Ng et al., 2025). Second, data for the most recent period (2025) are incomplete due to database indexing delays and the “citation lag” phenomenon, so the latest emerging trends may be underrepresented. Third, the descriptive bibliometric indicators used here, such as citation counts and burst strength, map research activity and structural evolution but are proxies for impact rather than direct measures of scientific quality or clinical validity. To address these constraints, future work should integrate semantic modeling and advanced network-based analyses to move beyond keyword co-occurrence, capture contextual nuances in scientific content, and more accurately trace knowledge dissemination across linguistic and disciplinary boundaries.

To address these limitations, future research could adopt complementary methodological strategies. Integrating semantic modeling techniques, such as natural language processing, with advanced network-based analyses would enable the capture of contextual and conceptual nuances in scientific content, moving beyond simple keyword co-occurrence. This approach would facilitate a more accurate tracing of knowledge dissemination across linguistic and disciplinary boundaries. Alternatively, future studies might employ the knowledge triangulation framework proposed by Kokol et al. (2018), which combines quantitative bibliometric mapping with qualitative synthesis. By integrating multiple sources of evidence, this framework provides a structured means to identify emerging research themes and latent knowledge structures that purely quantitative metrics could overlook.