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Channels (Austin)
Channels (Austin)
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1933-6950
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Taylor & Francis

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10.1080/19336950.2024.2396354
2396354
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Review Article
Review
Piezo1 channel: A global bibliometric analysis from 2010 to 2024
C. TIAN ET AL.
CHANNELS
https://orcid.org/0009-0006-9355-2614
Tian Chuanxi a *
https://orcid.org/0000-0001-7108-5687
Lyu Tianyi b *
https://orcid.org/0000-0001-9501-0743
Zhao Xirui c
https://orcid.org/0000-0003-4705-4201
Wang Ruoshui c
Wu Ying b †
Yang Daowen d †
a Traditional Chinese Respiratory Medicine, Beijing University of Chinese Medicine , Beijing, China
b Department of Acupuncture, Beijing Obstetrics and Gynecology Hospital, Capital Medical University , Beijing, China
c School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine , Beijing, China
d Department of Traditional Chinese Medicine for Pulmonary Diseases, China-Japan Friendship Hospital , Beijing, China
CONTACT Daowen Yang 13910331107@139.com
* These authors are contributed equally to this work

† These authors are contributed equally to this work

16 9 2024
2024
16 9 2024
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Integra05 9 2024
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20 8 2024
© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
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The Author(s)
https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

ABSTRACT

In recent years, the Piezo1 channel has attracted great attention. Piezo1’s research has made remarkable advance in many aspects. However, the overall trends and knowledge structures have not been systematically investigated from a worldwide viewpoint. Therefore, it is important to fill this knowledge gap and utilize a proper tool to show the research status, hotspots, and frontiers in the Piezo1 channel. In order to better investigate the hotspots and frontiers of the Piezo1 channel research, we retrieved relevant literature from Web of Science Core Collection (WoSCC) and applied CiteSpace to perform a bibliometric analysis. Our findings might serve as a reference for future research in this area.

KEYWORDS

Piezo1
pain
CiteSpace
visualization
Ministry of Science and Technology of the People´s Republic of China 2022YFC3500801 This work was supported by the Ministry of Science and Technology of the People´s Republic of China [2022YFC3500801].
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pmcIntroduction

Piezo1, a mechanically activated (MA) ion channel that converts mechanical force into chemoelectric signals, plays an essential role in a variety of biological processes [1]. It was first identified in 2010 to be a conserved eukaryotic MA ion channel that is involved in diverse mechanotransduction pathways such as touch sensation, proprioception, nociception, vascular development, and respiration [2,3]. In vitro studies have uncovered the structure of Piezo1 and how it functions in a native environment [3,4].

Strategies of targeting and modulating the Piezo1 channel have shown potential to produce significant therapeutic effects. Recent studies have demonstrated that Piezo1 is closely associated with diseases of various systems [5–9]. It was reported that Piezo1-mediated neurogenic inflammatory cascade exacerbated ventricular remodeling after myocardial infarction [5]. The Piezo1 channel was also found to regulate the antitumour cytotoxicity of T lymphocytes, enhancing the efficacy of cancer immunotherapies [6]. Previously published research has suggested that Piezo1 is a critical regulator of physiological and pathological endochondral ossification processes [7]. Besides demonstrating that its antagonists may be established as a novel approach to limit osteophyte formation in osteoarthritis (OA). It has been proposed that Piezo1 is pathologically upregulated in cardiovascular diseases via mechanical excitation [8], arrhythmia [9], and cardiomyopathy. Additionally, the Piezo1 channel is considered as a potential therapeutic target to treat COVID-19-associated endothelial dysfunction [10]. The activation of Piezo1 defines an essential event in B cell activation to membrane-presented antigens that might be exploited to improve the efficacy of vaccines [11].

In recent years, the Piezo1 channel has attracted great attention. Piezo1’s research has made remarkable advance in many aspects [3,12,13]. Due to the significant contribution on the recognition of Piezo ion channels for sensing mechanical stress, Ardem Patapoutian received the 2021 Nobel Prize [14,15]. However, the overall trends and knowledge structures have not been systematically investigated from a worldwide viewpoint. Therefore, it is important to fill this knowledge gap and utilize an proper tool to show the research status, hotspots, and frontiers on the Piezo1 channel.

Bibliometric analysis is an effective method to investigate research hotspots and the overall research trends in certain domains. In order to better grasp the hotspots and frontiers of Piezo1 channel, we retrieved the relevant literature from Web of Science Core Collection (WoSCC) and applied CiteSpace to perform a bibliometric analysis. Our findings might serve as a reference for future research in this area.

Data source and search

Web of science is the primary platform for scientific articles across various academic areas and is considered as the world’s most trusted database. To improve data representativeness and accessibility, our data were sourced from the Web of Science Core Collection (WoSCC). Since we know that the Piezo1 channel was first discovered in 2010, the data were downloaded from 1 January 2010 to 21 April 2024. The search strategy was [TS = Piezo-Type Mechanosensitive Ion Channel Component 1* OR Piezo1* OR Piezo1 channel*] AND [Language = (English)]. A total of 1456 publications were included, with the following publications excluded: early access (30), proceeding paper (6), meeting abstract (212), letter (19), news item (4), book chapters (17), retracted publication (1), editorial material (61), correction (15), and retraction (1). Finally, 1044 publications, including 895 articles and 148 reviews, were investigated. To avoid any potential fluctuations caused by the database’s daily updates, we completed our data search within one day. The CiteSpace 6.2.R4 was applied to visually display top countries. The CiteSpace 6.3.R1 was applied to visually display institutions, authors, keywords, research areas, and trends. Figure 1 shows the flow chart of data analysis. We collected the data directly from a public database, and no further clinical or animal trials are planned. Therefore, ethical approval was not required. Figure 1. Flow chart of Piezo1 channel researche inclusion.

According to the search strategy, 1456 publications were collected from the WoSCC. A total of 1044 publications were finally investigated, with 412 publications excluded. Citespace and Excel 2019 were used to visualize and analyze annual publications, countries/regions, institutions, authors, research areas, keywords, and keyword bursts.

Annual publication output

The number of publications indicates research speed and trends in this topic [16]. We performed a histogram to investigate the annual number of published papers, thus revealing the trends in the Piezo1 channel research. As shown in Figure 2, related research was first published in 2011. Since 2021, the number of publications began to exceed 100. From 2016 to 2024, the annual number has been growing rapidly. These results demonstrated steady growth and increasing attention to the Piezo1 channel. Figure 3 illustrates that articles comprised 85.73% of publications, demonstrating a strong focus on original studies in the Piezo1 channel field. Figure 2. The number of annual publications on Piezo1 channel research from 2004 to 2020.

The first article was published in 2011. The number of annual publications continued to increase from 2011 to 2023. Until 21 April 2024, the number amounted to 96.

Figure 3. Document type. Blue represents articles, and orange represents reviews.

Among 1044 publication, 895 (85.73%) were articles and 148 (14.27%) were reviews.

Active countries and institutions

Researchers from 153 institutes and 46 countries/territories contributed to the development of Piezo1 channel research. As shown in Table 1, China was the most productive country (30.27%, 316), producing the most number of papers on the Piezo1 channel, followed by the United States (291, 18.645%) and England (67, 7.649%). The University of California System (45) was the leading scientific research institution, followed by the Howard Hughes Medical Institute (36) and Centre National de la Recherche Scientifique (35). A co-occurrence map assists researchers to find collaboration links and offers useful information about well-known research teams [17,18]. As shown in Figures 4 and 5, there were close collaborations among top countries and institutions, indicating that the communication and cooperation among countries or institutions are particularly important in the Piezo1 channel research. Figure 4. The network of countries engaged in Piezo1 channel research.

Researchers from 46 countries/territories contributed to the development of Piezo1 channel research. The top three countries were China, USA, and England. There were close collaborations among different countries/territories.

Figure 5. The network of institutions engaged in Piezo1 channel research.

Researchers from 153 institutes contributed to the development of Piezo1 channel research. The top three institutes were the University of California System, the Howard Hughes Medical Institute, and Centre National de la Recherche Scientifique. There were close collaborations among different institutes.

Table 1. The top 10 countries and institutions contributed to publication on Piezo1 channel research.

Rank	Country	Frequency	Institution	Frequency	
1	PEOPLES R CHINA	316	University of California System	45	
2	USA	291	Howard Hughes Medical Institute	36	
3	ENGLAND	67	Centre National de la Recherche Scientifique (CNRS)	35	
4	JAPAN	52	University of Leeds	33	
5	FRANCE	41	Harvard University	30	
6	GERMANY	40	Chinese Academy of Sciences	29	
7	AUSTRALIA	39	University of New South Wales Sydney	27	
8	ITALY	30	Institut National de la Sante et de la Recherche Medicale (Inserm)	27	
9	SOUTH KOREA	21	State University of New York (SUNY) System	26	
10	RUSSIA	14	Victor Chang Cardiac Research Institute	25	

Active authors

A total of 207 authors participated in the Piezo1 channel research. Table 2 lists the top10 researchers with the most published papers. Cox Charles D was the most productive author with a total of 19 publications, primarily on the structure and function of Piezo1 [19,20], followed by Patapoutian Ardem and Beech David J. Author co-occurrence maps can help researchers find possible collaborators by offering details on influential research groups and potential partners [17,18]. Figure 6 demonstrates active communications among productive researchers. Figure 6. The network of authors contributed to Piezo1 channel research.

There are 207 authors participated in the Piezo1 channel research. The top three productive authors were Cox Charles D, Patapoutian Ardem, and Beech David J. There close collaborations among different authors.

Table 2. The top 10 active authors in the Piezo1 channel research.

Rank	Author	Frequency	
1	Cox, Charles D	19	
2	Patapoutian, Ardem	17	
3	Beech, David J	17	
4	Sachs, Frederick	17	
5	Li, Jing	16	
6	Martinac, Boris	14	
7	Andolfo, Immacolata	14	
8	Gottlieb, Philip A	13	
9	Xiao, Bailong	12	
10	Bae, Chilman	8	

Research area analysis

Figure 7 shows the top 10 research areas that appeared in publications related to the Piezo1 channel. Expression, blood pressure, and protein are the top three areas of Piezo1 channel. Figure 7. The keyword clustering in the Piezo1 channel research.

There were 10 research areas that appeared in publications related to the Piezo1 channel, including expression, blood pressure, protein, red blood cells, ATP release, ion channel, merkel cells, ion channels, cancer, and mechanosensitive ion channel.

Keyword co-occurrence

Keywords were extracted from the 1044 publications, which are core contents and research themes of the publications. According to keyword co-occurrence analysis, researchers can understand the hotspots and frontiers in a certain field. Providing a reasonable description of research hotspots and burst keywords can represent research frontiers over a period of time [21].

As shown in Figure 8 and Table 3, the top 20 keywords were “piezo1,” “expression,” “activation,” “mutations,” “activated ion channel,” “ion channels,” “mechanotransduction,” “cells,” “architecture,” “mechanisms,” “channels,” “mechanism,” “pressure,” “stretch,” “blood pressure,” “proteins,” “touch,” “differentiation,” “calcium,” and “membrane.” Therefore, we summarized research hotspots in the following aspects. Figure 8. The analysis of keywords in the Piezo1 channel research.

A total of 204 keywords were listed. “piezo1”, “expression”, “activation”, “mutations”, “activated ion channel”, “ion channels”, “mechanotransduction”, “cells”, “architecture”, and “mechanisms” were the top 10.

Table 3. Top 20 keywords in terms of frequency in Piezo1 channels.

Rank	keywords	Frequency	Rank	keywords	Frequency	
1	piezo1	149	11	channels	68	
2	expression	125	12	mechanism	65	
3	activation	111	13	pressure	58	
4	mutations	110	14	stretch	58	
5	activated ion channel	103	15	blood pressure	58	
6	ion channels	91	16	proteins	53	
7	mechanotransduction	90	17	touch	52	
8	cells	87	18	differentiation	48	
9	architecture	85	19	calcium	46	
10	mechanisms	72	20	membrane	42	

Piezo1 channel activation

In 2010, researchers discovered a group of ion channels called Piezo [2]. It is important to investigate how Piezo channels work and when they open. Separate work from different researchers demonstrated that the Piezo1 channel was activated by various types of mechanical and chemical stimuli [22,23]. Yoda1 is a promising candidate which specially activates the Piezo1 channel [24]. Patapoutian demonstrated that plasma membrane could expand the blades of the Piezo1 channel, impacting channel activation [3]. Importantly GsMTx4 has been reported as a pharmacological modulator that specifically targets Piezo1, supporting the use of this channel in high throughput screens for pharmacological agents and diagnostic assays [25]. Furthermore, the Piezo1 channel is an inherently mechano-gated channel activated by mechanical force through the lipid bilayer according to the evolutionary conserved force-from-lipid principle similar to other mechanosensitive channels, including MSCs, MscL, TREK1/2, TRAAK, and OSCA/TMEM63 [26,27]. The Piezo1 channel is commonly considered to participate in the onset and progression of many diseases. Activation of Piezo1 channel downregulates renin in juxtaglomerular cells and contributes to blood pressure homeostasis [28]. The Piezo1 channel drives chondrocyte mechanical injury due to high membrane tension, and this threshold can be altered by factors that influence membrane prestress, suggesting that modulating Piezo1 activation might offer a novel approach for the prevention or treatment of osteoarthritis (OA) [29]. A GsMTx4-treated cartilage reveals a chondroprotective effect by inhibiting Piezo1 activation [7]. GsMTx4 has been shown to reduce chondrocyte damage and death, while also preventing inflammation-induced rarefication [30]. Although the effect of GsMTx4 has been proven in vitro and ex vivo models, more research is needed to investigate the effect of GsMTx4 on OA in vivo animal models and potential clinical applications.

Piezo1 channel mutation

The Piezo1 channel plays an essential role in a number of diseases. Originally, Piezo1 was found to be mutated in dehydrated hereditary stomatocytosis [31]. It was soon realized that these were gain-of-function mutations [32]. Piezo1 gain-of-function mutations were further found to be correlated with hepatic iron metabolism [33]. An indication that Piezo1 mutations might be involved in lymphatic and hematologic disorders. Recent studies have identified Piezo1 mutations in patients suffering from idiopathic erythrocytosis [34], myelodysplastic syndromes [35], hereditary anemia [36], lymphatic dysplasia [37], and congenital lymphedema [38]. Considering the fact that Piezo1 lacks a fully-resolved molecular architecture and specific ligand-binding mechanisms, the development of Piezo1 inhibitors to treat these diseases is still in early stages [30].

Piezo1 channel mechanotransduction

The Piezo1 channel is considered as fully specialized mechanosensors for mediating versatile mechanotransduction in a wide variety of cell types. It was reported that astrocytes utilized Piezo1-mediated mechanotransduction mechanisms to robustly regulate adult neurogenesis and cognitive functions [39]. Importantly, 2 recent studies revealed that Piezo1-mediated mechanotransduction enhanced bone formation through the CaMKII and TGF-β1 signaling pathway [40,41]. Piezo1-mediated mechanotransduction was also proven to promote cardiac hypertrophy by impairing calcium homeostasis [11,42]. These reports suggest that Piezo1-mediated mechanotransduction might give us a novel entry point for the diagnosis and treatment of orthopedic, cardiac, and neurological disorders. However, Piezo1 channel pharmacology is limited to low-affinity drugs that exhibit poor solubility and stability in the treatment of neurological disorders [43]. Only a small number of agonists and antagonists are available to treat cardiovascular diseases and OA. Additionally, previous studies also reported conflicting phenotypes of Piezo1-mediated cellular responses. Achieving the desired therapeutic outcome while avoiding potential toxic effects is a major challenge [30].

Piezo1 and blood pressure

In 2016, a new research identified the Piezo1 channel as a key regulator of flow-induced ATP release and subsequent activation of downstream signaling pathways with effects on blood pressure [44]. However, its role in modulating blood pressure remains rather elusive. Two hypotheses were proposed. Yang et al. demonstrated that the Piezo1 channel downregulated the renin expression in JG cells, subsequently a reduction of blood pressure [28]. Cui et al. suggested that the Piezo1 channel expressed on Ah-type baroreceptor and baroreceptive neurons in the NG and NTS, and that it played a key role in a sexual-dimorphic BP regulation under physiological and hypertensive conditions through facilitation of baroreflex afferent neurotransmission [45]. These two hypotheses are required in further studies to confirm. COMP (Cartilage Oligomeric Matrix Protein), a novel Piezo1 channel regulator that controls blood pressure, was found [46]. A COMP C-terminus might directly interact with the C-terminus of Piezo1, thus increasing cellular Ca2+ influx, eNOS activity, and nitric oxide production. Exploring the precise mechanism by which COMP regulates Piezo1 efficient ion conduction is still a challenge. Moreover, the Piezo1 channel plays a crucial role not only in blood pressure, but also in various aspects of vascular physiology. It also serves as a multifunctional force sensor that involves in blood and lymphatic vessel development, vascular tension, and remodeling [47,48]

Keyword burst

As shown in Figure 9, strong citation bursts were used to identify and analyze keywords in order to investigate frontiers and emerging trends of the Piezo1 channel. The time interval in which the burst keyword appeared is shown by the red line. The direction “pain” has great potential, as proven by the fact that the citation burst time of keyword “pain” (2022–2024, 4.75) has continued until 2024 and is still ongoing. Figure 9. Top 15 keywords with the strongest citation bursts.

Top 15 keywords revealed the frontiers and emerging trends of Piezo channel. The direction “mutation” had the highest strength score. The direction “pain” had great potential, as its burst time continued to 2024.

Piezo1 channel and pain

Pain is one of our fundamental emotional and sensory perceptions [49]. Pain and pain-related diseases are leading causes of disability and disease burden globally. 86 publications related to pain and Piezo1 were included, including 64 articles and 20 reviews. Giniatullin, Rashid is the most productive author with a total of 6 publications, followed by Patapoutian Ardem and Coste Bertrand. The top 5 WOS categories are biochemistry molecular biology, neurosciences, physiology, chemistry multidisciplinary, and multidisciplinary sciences. The most cited and relevant article, “Mechanically Activated Piezo Channels Mediate Touch and Suppress Acute Mechanical Pain Response in Mice” has 80 citations. It suggested that Piezo channels can mediate touch and indirectly suppress acute pain in mouse models [50]. Moreover, the Piezo1 channel is involved in the transmission of pain information. Recent studies demonstrated that Piezo1 upregulation and activation were associated with osteoarthritis pain [51], migraine [52], and pain after peripheral nerve injury [53].

Conclusion

Based on the WOSCC database, this study demonstrates the characteristics of Piezo1 channel research by bibliometric and visual analysis. Since 2022, the number of publications began to exceed 200. According to recent trends, the number of publications on Piezo1 research will continue to increase. Globally, China is the leading country in this field. Current research hotspots mainly include “Activation,” “mutation,” “mechanotransduction”, and “blood pressure.” More attention should be given to “pain,” since it might be the next popular direction in the Piezo1 channel research.

Our study provides a comprehensive overview of Piezo1 channel research by using high-quality literature and rigorous data statistics. Researchers in this field are able to predict research frontiers, find research hotspots, and discover possible collaborative opportunities. This article might also serve as a reference for organizations considering whether to continue financing a particular research team.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions statement

Writing – original draft: Chuanxi Tian and Tianyi Lyuv; analysis and interpretation of the data: Chuanxi Tian and Tianyi Lyu; Writing – review & editing: Daowen Yang, Xirui Zhao, and Ruoshui Wang. All authors read and approved the final manuscript.

Data availability statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.
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