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Войти в исследования Endocrine, metabolic & immune disorders drug targets · 2026
Research Hotspots, Trends, and Molecular Mechanisms of Diabetes and Sarcopenia: A Bibliometric and Bioinformatics Analysis.
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Chen Xuwu, Li Zijing, Zhou Tanyue, Wu Wenjuan, Chen Long, Chen Xiangyang, Wang Maoyuan
Аннотация
INTRODUCTION: The co-occurrence of diabetes mellitus (DM) and sarcopenia is increasingly recognized as a significant clinical challenge, yet the underlying molecular mechanisms and research landscape remain incompletely characterized.
METHODS: Relevant literature was retrieved from the Web of Science database, and bibliometric visualization was conducted using CiteSpace 6.2.R4 and VOSviewer 1.6.20. Genes associated with both diseases were obtained from the GeneCards and OMIM databases, and a protein-protein interaction network was constructed. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) functional enrichment analyses were performed. Bibliometric findings were cross-validated with molecular mechanisms to identify convergent evidence.
RESULTS: The number of publications and citation frequency in this field showed a significant upward trend. China, Japan, and the United States contributed 58.6% of research papers, with Kyoto Prefectural University of Medicine, Seoul National University, and other institutions as major contributors. Fukui Michiaki was the most productive author, and Nutrients was the primary journal. Research themes evolved from early studies on molecular pathological mechanisms to investigations of clinical phenotypes and complications, and further to nutritional interventions, exercise therapy, and population management. Bibliometric analysis identified "insulin resistance" as the second most frequent keyword (212 occurrences), correlating with bioinformatics identification of INS as the primary hub gene among 97 shared targets. Five core genes (INS, ALB, AKT1, IL6, TNF) were significantly enriched in PI3K/MAPK and inflammatory pathways, supporting bibliometric emphasis on chronic inflammation.
DISCUSSION: Integration of bibliometric and bioinformatics results highlights insulin signaling, chronic inflammation, and nutritional status as common mechanisms linking DM and sarcopenia. These findings support the translational potential of lifestyle interventions (nutrition and resistance exercise) and insulin-sensitizing or anti-inflammatory therapies. Future research should focus on experimental validation and the development of combination strategies targeting the identified molecular network.
CONCLUSION: This study constructed a comprehensive knowledge map for diabetes and sarcopenia research, systematically elucidating current research status, hot topics, and molecular mechanisms. The findings provide a scientific basis for developing joint prevention and treatment strategies and guiding future research directions.
METHODS: Relevant literature was retrieved from the Web of Science database, and bibliometric visualization was conducted using CiteSpace 6.2.R4 and VOSviewer 1.6.20. Genes associated with both diseases were obtained from the GeneCards and OMIM databases, and a protein-protein interaction network was constructed. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) functional enrichment analyses were performed. Bibliometric findings were cross-validated with molecular mechanisms to identify convergent evidence.
RESULTS: The number of publications and citation frequency in this field showed a significant upward trend. China, Japan, and the United States contributed 58.6% of research papers, with Kyoto Prefectural University of Medicine, Seoul National University, and other institutions as major contributors. Fukui Michiaki was the most productive author, and Nutrients was the primary journal. Research themes evolved from early studies on molecular pathological mechanisms to investigations of clinical phenotypes and complications, and further to nutritional interventions, exercise therapy, and population management. Bibliometric analysis identified "insulin resistance" as the second most frequent keyword (212 occurrences), correlating with bioinformatics identification of INS as the primary hub gene among 97 shared targets. Five core genes (INS, ALB, AKT1, IL6, TNF) were significantly enriched in PI3K/MAPK and inflammatory pathways, supporting bibliometric emphasis on chronic inflammation.
DISCUSSION: Integration of bibliometric and bioinformatics results highlights insulin signaling, chronic inflammation, and nutritional status as common mechanisms linking DM and sarcopenia. These findings support the translational potential of lifestyle interventions (nutrition and resistance exercise) and insulin-sensitizing or anti-inflammatory therapies. Future research should focus on experimental validation and the development of combination strategies targeting the identified molecular network.
CONCLUSION: This study constructed a comprehensive knowledge map for diabetes and sarcopenia research, systematically elucidating current research status, hot topics, and molecular mechanisms. The findings provide a scientific basis for developing joint prevention and treatment strategies and guiding future research directions.