Mapping the global research landscape of mitophagy in Parkinson's disease: a bibliometric and visualization analysis

This study primarily utilized the Web of Science Core Collection (WoSCC; Clarivate Analytics, USA)—the gold-standard multidisciplinary citation index encompassing over 34,000 peer-reviewed journals across 254 research categories since 1900—to ensure rigorous bibliometric analysis of high-impact scientific literature. (Platform access: https://www.webofscience.com/wos↗). To systematically map the global research landscape of mitophagy in PD, the following search formula was applied: TS = (Parkinson* OR PD) AND TS = (mitophagy OR "mitochondrial autophagy"). The search was limited to articles and reviews published up to December 2024. The final search was conducted on January 12, 2025, to ensure inclusion of the most recent publications and to prevent data bias due to database updates. A total of 1712 documents were retrieved.

The initial search yield was filtered to include only English-language publications. Editorial material, book chapters, early access, meeting abstract, proceeding paper, correction, letter, data paper, publication with expression of concern, and retracted publication were excluded. The final dataset comprised articles and reviews articles that specifically addressed aspects of mitophagy in the context of PD.

To strengthen the validity and multidimensional scope of our investigation, we employed several bibliometric tools to uncover trends and patterns within this field.

CiteSpace, a software developed by Chaomei Chen, was pivotal in visualizing the co-citation and co-authorship networks, as well as tracking the evolution of key terms within the field [28]. Our utilization of CiteSpace 6.4 R1 allowed us to delve into hotspots countries/regions, dual-map overlays of journals, keyword timelines, and co-citation analyses.

In conjunction with CiteSpace, VOSviewer, developed by Nees Jan van Eck and his team, was instrumental in the bibliometric network graph analysis [29]. In this study, we utilized VOSviewer (version 1.6.20; Centre for Science and Technology Studies, Leiden University, The Netherlands) to visualize the distribution of countries/regions, institutions, and journals, and to construct co-authorship and keyword co-occurrence networks. The clustering algorithm of VOSviewer, which is based on a similarity matrix and the VOS mapping technique, enabled the automated clustering process. We also employed Pajek (version 5.18; developed by Andrej Mrvar and Vladimir Batagelj, Faculty of Computer and Information Science, University of Ljubljana) in conjunction with VOSviewer. Pajek is an advanced tool for network analysis, specializing in the visualization and management of large-scale networks [30]. In our research, Pajek was used to calculate and optimize graph data and correlation networks, thereby enhancing the clarity and interpretability of the network visualizations.

To further enhance our analysis, we employed Bibliometrix, an R-based tool, to examine key bibliometric data [31]. For the visualization and predictive modeling of publication trends over time, including both annual and predicted publication volumes, we utilized OriginPro 2024 software (OriginLab Corporation, 2024).

This study is a bibliometric analysis, and all data were obtained from publicly available academic database. As the research did not involve human or animal experimentation, personal data collection, or sensitive information, ethical approval was not required. All data were aggregated and analyzed in compliance with database terms of use, copyright regulations, and academic integrity standards to ensure the transparency and reproducibility of the study.

Figure 2B presents a nonlinear fitting curve generated using OriginPro 2024 software, which models the logistic growth of annual publications in this field from 2007 to 2024. The curve, derived from logistic regression analysis, is displayed alongside the actual publication data points and exhibits a strong correlation with an R-Square value of 0.9422, indicating a reliable fit. It forecasts a sustained rise in the number of publications, estimating around 225 publications per year by 2040. This projection is depicted by a red curve, accompanied by a 95% prediction band and a 95% confidence band, which visually represent the uncertainty associated with the predictions by accounting for data variability.

The USA leads with the most publications (479, 30.35%) and a betweenness centrality of 0.58—more than double that of the second, England (0.24), and far above others. This highlights the USA's key role in the global research network and its significant impact on mitophagy research in PD. China, with 353 (22.37%) publications and an intermediary centrality of 0.13, also figures prominently, reflecting its growing impact on global scientific discourse. England (170, 10.77%) and Germany (122, 7.73%) further underscore the significant European contribution to this research domain. However, the lower intermediary centrality values for these countries/regions suggest that their role in bridging international collaborations could be further enhanced.

Figure 3C provides an overview of the top 9 countries/regions with the strongest citation bursts, sorted by the start time of their respective bursts. A citation burst signifies a period during which a country or a region's scientific publications receive a sudden and significant increase in citations. The USA began its significant burst in 2007, while China and India both demonstrate notable bursts from 2022 to 2024, with China's burst strength reaching 20.96. These bursts reflect critical periods of intense research activity and influence within the field.

Figure 3D presents the annual publication trends for the USA, China, and India, which are among the countries/regions with the highest publication volumes and significant citation bursts. The USA shows a consistent increase in publication numbers over the years, with fluctuations but an overall upward trend, peaking around 2022. China's trend shows a steady rise from 2018 onwards, aligning with the table data that indicates a period of rapid growth in research output and influence. India, starting with a lower base,shows a gradual increase in publications, with a more pronounced rise from 2020.

Figure 4 A presents an institutional collaboration network map generated using VOSviewer. This network comprises 180 institutions, each depicted as a node, selected based on having published at least five papers, while excluding those lacking partnerships with other institutions. The resultant chart delineates five distinct clusters, with each node's color corresponding to its specific group. Node sizes are proportional to the number of publications, which highlights institutions with higher research output. The thickness of the lines connecting the nodes reflects the extent of collaboration, with thicker lines signifying more frequent cooperative interactions. Upon analyzing the network, it is evident that certain institutions occupy central positions within the diagram, such as McGill University, University College London, University of Pittsburgh, Mayo Clinic, and the National Institute of Neurological Disorders and Stroke. This indicates their crucial role in the overall collaborative network. These central nodes, distinguished by their larger size and numerous connections, likely represent key research hubs actively involved in knowledge exchange and joint research initiatives. Furthermore, it is apparent that institutions with close collaborative relationships predominantly belong to the same country.

Figure 4B presents a network map with nodes identical in size and spatial arrangement to those in Fig. 4A. Unlike Fig. 4A, the color of the nodes in Fig. 4B reflects the average year of publication. Nodes displaying red tones indicate more recent academic contributions. The network shows that the nodes on the periphery of the collaboration network, many of which represent Chinese institutions, exhibit a deeper red hue; this suggests that these institutions have been quite active recently in the research area of mitophagy in PD.

When discussing the significance of journal distribution in the field of mitophagy in PD, Bradford's Law offers a crucial perspective. Bradford's Law, introduced by Samuel C. Bradford, describes a specific pattern of journal distribution within scientific literature. According to this law, if journals are sorted by the number of papers they publish on a particular subject, they can be divided into several zones, with each zone containing an equal number of papers, while the number of journals in each zone decreases geometrically, meaning a small number of core journals account for the majority of publications [32].

Table 3 presents the top 10 journals by number of publications, co-citation frequency, impact factor (IF;JCR 2024), and JCR quartile. Autophagy tops the list with 55 publications and an IF of 14.3, ranking in JCR Q1.

Figure 7B focuses on the average normalized citations (avg. norm. citations) metric, visualized by color intensity. Deeper red indicates a higher frequency of being cited, while bluer hues signify lower citation rates. Journals like Nature, Journal of Cell Biology, Molecular Cell, Ageing Research Reviews and Neuron appear in deep red, denoting higher average citation counts and thus prominent status and broad impact.

Table 7 presents the top 10 most cited references. These references were identified using CiteSpace software, with the "Look Back Year (LBY)" parameter set at 5 years. This means that CiteSpace considered the citation status of each paper within 5 years after its publication. The purpose of this setting is to focus more precisely on recent research advancements and streamline the analysis network. By limiting the analysis to the most recent 5 years, we aim to identify papers that have garnered significant attention shortly after their publication, rather than those that have accumulated citations over a longer period. This approach helps to more accurately reflect the current research landscape and identify key papers that are driving recent trends. However, it is also worth noting that this setting may exclude some early foundational articles in the field. For example, the seminal work by Valente et al. on the identification of mutations in PINK1 as a cause of hereditary early-onset Parkinson's disease is a foundational study in this field [9]. Similarly, Clark et al. demonstrated the role of Drosophila PINK1 in mitochondrial function and its genetic interaction with parkin [52], while Park et al. further elucidated the mitochondrial dysfunction in Drosophila PINK1 mutants and how it can be complemented by parkin [53]. These early studies laid the groundwork for understanding the role of PINK1 in PD but may not be included in our analysis due to the 5-year LBY parameter. Despite this potential limitation, the current analysis still provides valuable insights into the most impactful recent research in the field.

Among these highly cited papers, 90% are original research articles. A significant portion of these highly cited publications overlaps with the previously mentioned top 15 highly cited publications (see Table 6), highlighting their importance and representativeness.

Figure 16B highlights the top 25 references with the strongest citation bursts. The first two bursts occurred in 2009, with papers titled "Parkin is recruited selectively to impaired mitochondria and promotes their autophagy" [50] and "The PINK1/Parkin pathway regulates mitochondrial morphology" [54]. Notably, the paper by Narendra et al. has the strongest burst (strength = 64.35) and its burst duration lasted until 2013. Another high-burst paper is "The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy" by Lazarou et al. (strength = 61.16) [48]. The data shows that papers published in 2010 caused the most citation bursts (seven in total), indicating a surge in related research activities.

Our study identified relevant literature starting from 2007 by using the search terms TS = (Parkinson* OR PD) AND TS = (mitophagy OR "mitochondrial autophagy"). It is important to note that foundational studies in the field of mitophagy date back to the 1990s. For instance, the initial reports of mutations in the PRKN and PINK1 genes [9, 10]. provided crucial insights into the genetics of PD. Additionally, research in Drosophila melanogaster elucidated the functional interaction between PRKN and PINK1 in a common pathway [52, 55], which is now recognized as a key component of mitophagy. These early studies laid the groundwork for subsequent research on mitophagy and have significantly influenced the development of the field. Although our main analysis focuses on research trends from 2007 onwards to capture recent developments, the seminal contributions of these early studies must be acknowledged.

In this study, we utilized a nonlinear fitting curve to elucidate the annual publication growth trajectory of mitophagy research in PD. This trend aligns with the theory of scientific development proposed by Derek J. de Solla Price [56], which posits that the volume of scientific literature in a particular field will initially exhibit exponential growth before eventually plateauing. Notably, the inflection point of this growth pattern can be traced back to around 2010, a period during which key breakthrough studies laid the foundation for the subsequent establishment of paradigms. For instance, Narendra et al. revealed the mechanism by which PINK1 accumulates on damaged mitochondria and how this accumulation triggers the recruitment of Parkin and mitophagy [36]. Additionally, the team of Vives-Bauza elucidated how PINK1 and Parkin jointly regulate mitochondrial transport and aggregation, facilitating autophagic degradation in the perinuclear region [41]. These studies provided the molecular framework for the subsequent rapid growth phase of publications. The current surge in publication numbers indicates that the field has established a dominant paradigm and is in the application phase, characterized by the rapid expansion of knowledge and the widespread dissemination of established theories and methods. This period has benefited from recent in-depth research on PD-related mitochondrial dysfunction, such as the discovery of the interaction between α-synuclein and mitochondria[57], as well as technological advancements like CRISPR gene editing [58]. Moreover, policy funding has also been a powerful driving force behind the expansion of this field. By using the search term ("parkinson's disease" AND "mitophagy") to access the official NIH RePORTER database (https://reporter.nih.gov↗), we obtained funding data from 2007 to 2024. The initial funding in 2007 was 5.8 million dollars, which increased to 25 million dollars in 2010 (+ 331%). During the technological breakthrough period from 2011 to 2017, the average annual growth rate was 34.6%, peaking at 853 million dollars in 2017. From 2018 to 2023, during the clinical translation phase, the funding amounts stabilized in the range of 470 to 790 million dollars, reflecting a sustained shift in strategic focus towards therapeutic development. The influence and recognition of scientific literature will accumulate over time and eventually stabilize. As shown in Fig. 2B, the annual publication trend curve for PD-related mitophagy research is flattening. However, these predictions should be treated with caution. Although the nonlinear fitting curve provides robust predictions based on historical data, the dynamic and complex nature of scientific research cannot be overlooked. Actual trends may be influenced by a variety of internal and external factors. External factors include changes in research funding, policy adjustments, or global events, all of which can impact the scientific publication process. Internal factors involve technological advancements in related fields, the evolution of research methods, or shifts in the academic community's research focus.

The analysis of global research collaboration on mitophagy in PD reveals a dynamic interplay of productivity, influence, and regional specialization.

The United States serves as the central hub of global Parkinson's research collaboration, reflected in its leading publication volume (479), betweenness centrality (0.58), and total link strength (312). Seminal work established the PINK1-Parkin axis: Narendra et al. [36] described PINK1 stabilization on depolarized mitochondria as a critical trigger for Parkin recruitment, complemented by Matsuda [19] showing that PINK1-dependent mitochondrial localization releases Parkin's latent ubiquitin ligase activity. Youle and Narendra [22] synthesized these mechanisms into an evolutionary conserved framework for mitochondrial quality control. Subsequent investigations expanded this paradigm: Chen [45] identified mitofusin 2 (Mfn2) as a PINK1-phosphorylated Parkin receptor, Zhang et al. [59] revealed BNIP3's role in stabilizing full-length PINK1 to facilitate Parkin recruitment, and Harbauer et al. [60] uncovered neuron-specific PINK1 mRNA trafficking via SYNJ2/SYNJ2BP for local mitophagy activation. Regulatory mechanisms were further elucidated by Bingol et al. [61], who characterized USP30 as a deubiquitinase antagonizing Parkin-mediated ubiquitylation, Heo et al.[62] detailing the TBK1-dependent amplification cascade via OPTN/NDP52 recruitment, and Fiesel et al. [63] demonstrating that the PINK1-G411A substitution enhances ubiquitin phosphorylation kinetics and mitophagy efficiency through optimized substrate receptivity. Pathophysiological connections were robustly characterized: Hsieh et al. [64] linked impaired Miro degradation to defective mitophagy in familial and sporadic PD using iPSC-derived neurons, while Grassi et al. [65] identified neurotoxic Pα-syn* aggregates inducing mitochondrial damage and fragmentation that trigger Parkin-dependent mitophagy. These mechanistic insights directly informed therapeutic development: Fang et al. [66] validated that USP30 knockout or pharmacologic inhibition protects dopaminergic neurons in α-synucleinopathy models. While China ranks second in productivity (353 publications), its relatively low betweenness centrality (0.13) and total link strength (102) suggest a focus on domestic or regionally clustered research, indicating a need for deeper integration into global networks. The citation bursts observed in China (2022–2024, strength = 20.96) and India (2022–2024, strength = 14.3) signal shifting dynamics (Fig. 3C). China's surge aligns with its strategic investments in neurodegenerative research. In recent years, Chinese scholars have made significant contributions to elucidating the molecular mechanisms and therapeutic strategies targeting mitophagy in PD. In the context of core regulatory pathways, Wang et al. revealed that PTEN-L acts as a novel phosphatase to inhibit PINK1-Parkin-mediated mitophagy through ubiquitin dephosphorylation [67]. Complementary studies by Huang et al. and Niu et al. further demonstrated the critical roles of metabolic enzymes (PANK2) [68] and deubiquitinating regulators (USP33) [69] in modulating PINK1-Parkin signaling, highlighting the dynamic interplay between ubiquitination and mitochondrial quality control. Regarding mitochondrial dynamics, the Chen team systematically established the involvement of Drp1-mediated fission in paraquat-induced neuronal damage [70, 71], while Han et al. identified PINK1-dependent phosphorylation of Drp1 at Ser616 as a key modulator of mitochondrial morphology [72]. In therapeutic development, Liu et al. reported that lovastatin enhances SHP2-mediated mitophagy to alleviate parkinsonism in murine models [73]. Innovative nanotechnology-driven approaches, such as sequence-targeted lycopene nanodots [74] and single-atom nanocatalytic platforms [75], were designed to promote pro-survival mitophagy and suppress neuroinflammation, respectively. Epigenetic studies uncovered non-coding RNA networks, including the circEPS15/miR-24-3p axis [76] and LncRNA NR_030777 [71], which regulate mitophagy through ATG12 and CDK1 pathways. Notably, Bao et al. proposed a non-canonical mitochondrial quality control mechanism involving mitolysosome exocytosis [77], whereas Zhang et al. and Han et al. elucidated crosstalk between mitophagy and ferroptosis via NKAα1 inhibition [78] and Nrf2-mediated lipid peroxidation regulation [79]. These findings collectively provide a multifaceted framework for understanding PD pathogenesis and advancing mitochondrion-targeted therapies.

India's growth, though starting from a smaller base, reflects rising interest in PD epidemiology and cost-effective therapeutic strategies, such as repurposed mitochondrial enhancers. Annual publication trends (Fig. 3D) further highlight this geographic diversification: the U.S. maintains steady growth, China exhibits exponential output since 2018, and India shows accelerating contributions post-2020.Recent years have witnessed significant progress from Indian researchers in understanding mitophagy regulation and therapeutic applications in PD. By establishing drosophila models, studies revealed that Rab11 modulates mitochondrial quality control through the Parkin/PINK1 signaling pathway [80]. Rodent studies demonstrated that pharmacological inhibition of deubiquitinating enzyme USP14 markedly amplified mitophagic activity and alleviated dopaminergic neurodegeneration [81]. Furthermore, SH-SY5Y cell-based investigations elucidated that andrographolide suppresses NLRP3 inflammasome activation via Parkin-mediated mitophagy [82]. These findings collectively unravel the complexity of mitophagic networks, providing experimental foundations for developing targeted nanodelivery systems and epigenome-modulating strategies.

In Europe, England (170 publications) and Germany (122 publications), demonstrate strong collaboration (total link strengths of 188 and 153, respectively). However, their relatively lower centrality values compared to USA highlight a gap in facilitating cross-regional knowledge exchange. England's key studies include. Ziviani et al. [83] demonstrate conserved PINK1-dependent mitofusin ubiquitination in Drosophila models. Lee et al. [84] challenge prevailing paradigms by documenting persistent basal mitophagy in Pink1/parkin-null organisms, despite progressive PD pathology. Usher et al. [85] further validate non-canonical phospho-ubiquitin turnover independent of autophagy machinery. Essential regulatory components are further defined through Burchell et al. [86] who demonstrate Fbxo7-Parkin interactions critical for mitophagy initiation in PARK15-linked PD, while Martinez et al. [87] identify CISD1 inhibition as a therapeutic strategy to rescue PD-associated mitophagy failure. German research has systematically delineated the regulatory network and pathological mechanisms of the PINK1/Parkin pathway in PD. The Geisler group demonstrated that PD-associated PINK1/Parkin mutations impair mitophagy, leading to accumulation of damaged mitochondria [88]. Meissner et al. identified the mitochondrial protease PARL as a negative regulator that cleaves PINK1 [89], while the Burbulla team revealed that mortalin deficiency triggers mitochondrial proteotoxic stress and activates the unfolded protein response (UPR(mt)), which can be rescued by Parkin/PINK1 overexpression [90]. Mueller-Rischart reported a non-mitophagic function of Parkin, showing it maintains mitochondrial integrity via linear ubiquitination of NEMO to activate NF-κB signaling[91]. Regarding disease progression, Borsche's cohort study established that PRKN/PINK1 mutations induce mtDNA release and cGAS-STING-mediated inflammation, validating serum IL-6 and circulating cell-free mtDNA as diagnostic and progression biomarkers [92], whereas Torres-odio demonstrated in mouse models that PINK1 deficiency drives temporal pathology cascades—from early spliceosome dysfunction and mid-stage ubiquitin–proteasome dysregulation to late neuroinflammation [93]. For therapeutic targeting, Polachova developed PARL-specific ketoamide inhibitors to activate PINK1/Parkin-dependent mitophagy [94], and Roverato proposed inhibiting the inflammation-induced FAT10-Parkin axis to restore mitochondrial clearance [95].

From the perspective of institutional distribution, research on mitophagy in PD exhibits a multipolar pattern, yet with significant geographical concentration. Institutions from North America and Europe dominate the field, with four US institutions ranking in the top ten (National Institute of Neurological Disorders and Stroke[NINDS], University of Pittsburgh, Mayo Clinic, and Johns Hopkins University). Collectively, these institutions account for 51.2% of the total citations among the top ten, with NINDS alone amassing 10,427 citations, thereby underscoring its academic leadership. Among European institutions, University College London (UCL) stands out as a core hub in the global collaborative network, with a total link strength of 128. Its extensive collaborations likely stem from the integration of clinical resources and fundamental research capabilities.

As depicted in the institutional collaboration network (Fig. 4A), institutions such as University College London (total link strength of 128) and the Mayo Clinic (total link strength of 99) occupy core hub positions. Their extensive collaborative ties indicate that the deep integration of clinical and basic research is pivotal in driving the translation of mitophagy research into therapeutic strategies. However, the collaboration network remains predominantly intra-national clusters (e.g.,US and German institutions forming distinct clusters), suggesting that geographical proximity and shared research funding systems may still be the primary drivers of collaboration, despite the global demand for PD research. The increased activity of Chinese institutions in recent years is evidenced by the concentrated distribution of red nodes (representing recent publications) in Fig. 4B. The Chinese Academy of Sciences (CAS, 29 publications) stands as a representative of China's research productivity, ranking sixth globally in terms of publication output. It should be noted that the literature inclusion threshold of VOSviewer (≥ 5 publications) may underestimate the collaborative potential of emerging institutions,as there may be initial collaborations in the actual research network that are not visualized.

For researchers newly entering the field of mitophagy in PD, priority should be given to core institutions with sustained high productivity. For instance, McGill University (with 52 publications) and University College London (with 45 publications) not only maintain stable research output but also their high total link strength (84 and 128, respectively) indicates that their achievements are mostly generated in a collaborative innovation environment. Particular attention should be paid to the 27 publications from the National Institute of Neurological Disorders and Stroke (NINDS), with an average citation per paper reaching 386 times, in order to comprehend the core theoretical framework of the field. Based on the bibliometric analysis results, a multi-dimensional strategy should be adopted when selecting collaborative teams. First, high-link-strength hub institutions should be identified, with priority given to teams with a total link strength greater than 80 and an average annual publication output exceeding five papers (such as University College London and the University of Tübingen). These institutions are characterized by dense node connection lines and spanning multiple research clusters in the collaboration network depicted in Fig. 4A. Second, highly active institutions should be tracked, with a focus on red nodes in Fig. 4B that have an average publication year after 2018, such as the Chinese Academy of Sciences, which has shown a significant fluctuating upward trend in publication output between 2018 and 2022. Finally, the compatibility of international cooperation should be assessed, with teams that have at least five co-authored papers with international partners being selected. It is recommended that new researchers prioritize teams with a total link strength higher than 50 and a record of transnational co-authorship in the past three years when choosing institutions, in order to enhance the visibility and translational efficiency of research outcomes. By integrating the three dimensions of institutional influence, technical complementarity, and cooperation maturity, researchers can systematically optimize their team selection decisions.

The journal analysis shows that mitophagy research in PD is highly concentrated, with 22 core journals (Zone 1) accounting for most publications. Autophagy (IF = 14.3,Q1) stands out with 55 publications, establishing its authority in mitophagy research. Figure 7A maps the core structure of PD mitophagy research. The red, blue, and green clusters are evenly distributed, signifying their equal importance. The red cluster represents molecular neurobiology, the blue cluster focuses on autophagy mechanisms, and the green cluster pertains to PD genetics and pathology. In contrast, the smaller yellow cluster, located between the red and blue clusters, emphasizes PD translational research, serving as a bridge that connects fundamental mechanisms with disease pathology. The yellow nodes, which symbolize elements of translational research, are interspersed throughout the main clusters, underscoring the robust connections between translational research and other critical areas of study.

Notably, top-tier interdisciplinary journals like Nature, despite their relatively low volume of publications (Fig. 7B), often feature breakthrough studies, as indicated by their high average normalized citation rates (deep red nodes). Nature's research on mitophagy in PD has been pivotal in integrating molecular mechanisms, pathological associations, and targeted therapies. Seminal studies include the elucidation of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization [96], genome-wide RNAi screens identifying regulators of parkin upstream of mitophagy [97], and the role of USP30 in opposing parkin-mediated mitophagy [61]^. Structural studies have detailed the activation mechanism of Parkin by phosphorylated ubiquitin [98], the interaction mode of PINK1 with ubiquitin [99], and the mechanism of Parkin activation by PINK1 [100]. These studies have precisely explained the mechanisms of early-onset PD mutations. Research has also expanded into the gut-brain axis, revealing how intestinal infections can trigger neuronal immune attacks via mitochondrial antigens [101]. Cryo-electron microscopy capturing the full activation pathway of PINK1 [102] provides an atomic-level blueprint for targeted interventions. In contrast, high-volume journals like Autophagy focus more on in-depth analysis of mechanistic details, forming a complementary pattern where top-tier journals set the direction and specialized journals deepen the research.

As shown in Fig. 9, the actual distribution of author productivity significantly deviates from Lotka's Law, with a much higher proportion of authors contributing only one publication (78.6% vs. the predicted 62%). This suggests a large number of short-term participants or interdisciplinary collaborators. This pattern may result from the need to integrate knowledge across multiple disciplines, such as neurodegenerative disease mechanisms, cell biology, and molecular genetics. Additionally, the high average number of co-authors per publication (6.9) suggests a strong collaborative structure, leading to more one-time contributors. Among authors with two or more publications, the actual proportions are consistently lower than Lotka's Law predictions, indicating a highly concentrated core research group in the field.

The research area is marked by a collaborative network centered on key scholars and institutions. Hattori N from Juntendo University and Youle RJ from the National Institute of Neurological Disorders and Stroke (NINDS) have emerged as cornerstones of the field. Hattori N has published 28 papers, which account for a significant proportion of Juntendo University's total publications in this area (totaling 34 papers). His extensive internal collaborations within the university have played a crucial role in shaping the institution's overall contributions to the field. Meanwhile, Youle RJ's work has been highly influential, with a citation count of 12,235. Hattori N's team focuses on the roles of PINK1 and Parkin genes in PD and their functions in mitochondrial quality control. Their studies have revealed that PINK1 phosphorylates the ubiquitin-like domain (Ubl) of Parkin upon loss of mitochondrial membrane potential, promoting Parkin translocation to and activation on mitochondria, thereby triggering mitophagy [103]. They also found that mitochondrial dysfunction caused by PINK1 deficiency is associated with defects in the respiratory chain rather than proton leak [104]. In animal models, Hattori N further confirmed that Parkin deficiency impairs mitochondrial turnover and leads to dopaminergic neuronal loss [105]. Youle RJ's team has elucidated the critical mechanisms of PINK1 and Parkin in regulating mitophagy [36]. They discovered that PINK1 stability is regulated by mitochondrial membrane potential and identified several proteins regulating the PINK1/Parkin pathway, such as TOMM7, HSPA1L, and BAG4 [97]. They also found that Rab protein cycling in the endoplasmic reticulum plays an important role in Parkin-mediated mitophagy [106]. These findings have advanced our understanding of PD pathogenesis and laid a solid foundation for the field. Notably, the institutional distribution shows that McGill University (with Fon EA and Trempe JF) and Mayo Clinic (with Springer W and Fiesel FC) each have two scholars in the top ten. Their total link strengths (184/120 for McGill University and 273/256 for Mayo Clinic) are relatively high, indicating stable and efficient collaborative mechanisms within these institutions.

The co-authorship network map (Fig. 10A) shows a hierarchical structure with scholars like Hattori N, Youle RJ, Springer W, and Fon EA as central hubs. These researchers have published at least 20 papers each and connect multiple clusters, acting as bridges in cross-team collaborations. Emerging peripheral networks represent potential research frontiers, such as new genetic regulators or therapeutic targets. These groups, though currently small, may play a pivotal role in future research and require sustained funding and mentorship to enhance their impact. Figure 11B highlights Youle RJ's dominance through a color gradient of average normalized citations (darker red indicates higher impact). Node colors also reflect differences in research timelines: Fon EA and Trempe JF have redder nodes (more recent publications), while Youle RJ and Springer W have bluer nodes (earlier publications).

Collaboration and institutional support are key to advancing research in this field. While top scholars have made significant contributions, emerging researchers and small teams need support to prevent knowledge gaps. Interdisciplinary integration can improve research efficiency and address the complexity of PD pathogenesis.