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已发表论文
绘制知识图谱：代谢功能障碍相关脂肪性肝病机制的 20 年文献计量分析
Authors Huang JW, Man NX, Wang HX, Ai XT, Wei DL, Dai YK
Received 21 August 2025
Accepted for publication 18 November 2025
Published 3 December 2025 Volume 2025:17 Pages 177—198
DOI https://doi.org/10.2147/HMER.S562237
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Gerry Lake-Bakaar
Jia-Wei Huang,1 Ng Xin Man,1 Hong-Xin Wang,2 Xiang-Ting Ai,1 Dan-Lei Wei,1 Yun-Kai Dai3
1The Affiliated Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510130, People’s Republic of China; 2School of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong, 510632, People’s Republic of China; 3Department of Gastroenterology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510130, People’s Republic of China
Correspondence: Dan-Lei Wei, The Affiliated Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510130, People’s Republic of China, Email 939762912@qq.com Yun-Kai Dai, Department of Gastroenterology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510130, People’s Republic of China, Email yun-kaidai@hotmail.com
Background and Purpose: Metabolic dysfunction-associated steatotic liver disease (MASLD), affecting between 20% and 30% of adults around the world, represents a growing public health burden characterized by hepatic steatosis concurrent with cardiometabolic risk factors. Despite two decades of research into its pathophysiology – spanning insulin resistance, gut-liver axis dysregulation, and genetic/epigenetic mechanisms – the vast body of literature has not yet been systematically mapped. A comprehensive bibliometric analysis mapping the field’s evolution, collaborative networks, and knowledge gaps remains lacking. Therefore, a 20-year bibliometric analysis (2005– 2024) on the mechanism of MASLD was conducted.
Patients and Methods: Publications on the mechanisms of MASLD were retrieved from the Web of Science Core Collection. The search period spanned from January 1st, 2005 to December 31st, 2024. Data were analyzed with CiteSpace (v6.3.R1) and VOSviewer (v1.6.20) to assess publication trends, country/institution contributions, journal influence, author networks, keyword clusters, and reference co-citations.
Results: China (40.75% of publications, n=4368) and the USA (21.18%, n=2270) dominate research output, with the Chinese Ministry of Education, Shanghai Jiao Tong University, and Harvard University as top institutions. International collaboration is prominent, particularly between China and the USA. International Journal of Molecular Sciences, Nutrients, and high-impact journals (Journal of Hepatology, IF=33.0) are key publication venues. Keyword analysis identifies five major research clusters: (1) lipid metabolism/mitochondrial dysfunction, (2) dietary factors/exercise, (3) inflammation/fibrosis, (4) metabolic comorbidities, and (5) gut-liver axis dysregulation. Temporal trends reveal a shift from insulin resistance/oxidative stress toward microbiota and molecular drivers (eg, WDR6-PPP1CB). Influential authors include Nobili Valerio (most productive) and Gerald I. Shulman (most cited; n=7703). Reference bursts highlight seminal works on disease burden (Younossi 2016) and pathogenesis (Powell 2021, Friedman 2018).
Conclusion: This first comprehensive bibliometric analysis of MASLD mechanisms highlights dynamic growth, interdisciplinary collaboration, and evolving research hotspot. Persistent challenges include mechanistic heterogeneity, early diagnostic tools, and targeted therapies. In conclusion, this analysis provides a foundational roadmap for researchers and policymakers, highlighting the imperative to translate mechanistic insights into precision diagnostics and therapies to mitigate the growing global burden of MASLD.
Keywords: bibliometrics, metabolic dysfunction-associated steatotic liver disease, mechanism, therapy
1The Affiliated Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510130, People’s Republic of China; 2School of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong, 510632, People’s Republic of China; 3Department of Gastroenterology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510130, People’s Republic of China
Correspondence: Dan-Lei Wei, The Affiliated Guangzhou Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510130, People’s Republic of China, Email 939762912@qq.com Yun-Kai Dai, Department of Gastroenterology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510130, People’s Republic of China, Email yun-kaidai@hotmail.com
Background and Purpose: Metabolic dysfunction-associated steatotic liver disease (MASLD), affecting between 20% and 30% of adults around the world, represents a growing public health burden characterized by hepatic steatosis concurrent with cardiometabolic risk factors. Despite two decades of research into its pathophysiology – spanning insulin resistance, gut-liver axis dysregulation, and genetic/epigenetic mechanisms – the vast body of literature has not yet been systematically mapped. A comprehensive bibliometric analysis mapping the field’s evolution, collaborative networks, and knowledge gaps remains lacking. Therefore, a 20-year bibliometric analysis (2005– 2024) on the mechanism of MASLD was conducted.
Patients and Methods: Publications on the mechanisms of MASLD were retrieved from the Web of Science Core Collection. The search period spanned from January 1st, 2005 to December 31st, 2024. Data were analyzed with CiteSpace (v6.3.R1) and VOSviewer (v1.6.20) to assess publication trends, country/institution contributions, journal influence, author networks, keyword clusters, and reference co-citations.
Results: China (40.75% of publications, n=4368) and the USA (21.18%, n=2270) dominate research output, with the Chinese Ministry of Education, Shanghai Jiao Tong University, and Harvard University as top institutions. International collaboration is prominent, particularly between China and the USA. International Journal of Molecular Sciences, Nutrients, and high-impact journals (Journal of Hepatology, IF=33.0) are key publication venues. Keyword analysis identifies five major research clusters: (1) lipid metabolism/mitochondrial dysfunction, (2) dietary factors/exercise, (3) inflammation/fibrosis, (4) metabolic comorbidities, and (5) gut-liver axis dysregulation. Temporal trends reveal a shift from insulin resistance/oxidative stress toward microbiota and molecular drivers (eg, WDR6-PPP1CB). Influential authors include Nobili Valerio (most productive) and Gerald I. Shulman (most cited; n=7703). Reference bursts highlight seminal works on disease burden (Younossi 2016) and pathogenesis (Powell 2021, Friedman 2018).
Conclusion: This first comprehensive bibliometric analysis of MASLD mechanisms highlights dynamic growth, interdisciplinary collaboration, and evolving research hotspot. Persistent challenges include mechanistic heterogeneity, early diagnostic tools, and targeted therapies. In conclusion, this analysis provides a foundational roadmap for researchers and policymakers, highlighting the imperative to translate mechanistic insights into precision diagnostics and therapies to mitigate the growing global burden of MASLD.
Keywords: bibliometrics, metabolic dysfunction-associated steatotic liver disease, mechanism, therapy