Background: Diabetes has a substantial impact on public health, highlighting the need for novel treatments. Ubiquitination, an intracellular protein modification process, is emerging as a promising strategy for regulating pathological mechanisms. We hypothesize that ubiquitination plays a critical role in the development and progression of diabetes and its complications, and that understanding these mechanisms can lead to new therapeutic approaches.
Aim: To uncover the research trends and advances in diabetes ubiquitination and its complications, we conducted a bibliometric analysis.
Methods: Studies on ubiquitination in diabetes mellitus and its complications were retrieved from the Web of Science Core Collection. Visual mapping analysis was conducted using the CiteSpace software.
Results: We gathered 791 articles published over the past 23 years, focusing on ubiquitination in diabetes and its associated complications. These articles originated from 54 countries and 386 institutions, with China as the leading contributor. Shanghai Jiao Tong University has the highest number of publications in this field. The most prominent authors contributing to this research area include Wei-Hua Zhang, with Zhang Y being the most frequently cited author. Additionally, is noted as the most cited in this field. The predominant keywords included expression, activation, oxidative stress, phosphorylation, ubiquitination, degradation, and insulin resistance.
Conclusion: The role of ubiquitination in diabetes and its complications, such as diabetic nephropathy and cardiomyopathy, is a key research focus. However, these areas require further investigations.
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http://dx.doi.org/10.4239/wjd.v16.i1.100099 | DOI Listing |
World J Diabetes
January 2025
College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei 230012, Anhui Province, China.
Background: Diabetes has a substantial impact on public health, highlighting the need for novel treatments. Ubiquitination, an intracellular protein modification process, is emerging as a promising strategy for regulating pathological mechanisms. We hypothesize that ubiquitination plays a critical role in the development and progression of diabetes and its complications, and that understanding these mechanisms can lead to new therapeutic approaches.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Nephrology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang, 310000, PR China.
Background: Ferroptosis plays an important role in the development of diabetic nephropathy (DN). However, its specific regulatory mechanisms remain unclear.
Methods: MPC5 cells were cultured in high glucose (HG) medium to stimulate the HG environment in vitro.
EMBO J
January 2025
Division of Neurology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Polyglucosans are glycogen molecules with overlong chains, which are hyperphosphorylated in the neurodegenerative Lafora disease (LD). Brain polyglucosan bodies (PBs) cause fatal neurodegenerative diseases including Lafora disease and adult polyglucosan body disease (ABPD), for which treatments, biomarkers, and good understanding of their pathogenesis are currently missing. Mutations in the genes for the phosphatase laforin or the E3 ubiquitin ligase malin can cause LD.
View Article and Find Full Text PDFJ Steroid Biochem Mol Biol
January 2025
Department of endocrinology, the Second People's Hospital of Kunming, Kunming 650203, Yunnan, PR China. Electronic address:
The disorders of glucose and lipid metabolism contribute to severe diseases, including cardiovascular disease, diabetes, and fatty liver. Here, we identified DNA damage-binding protein 2 (DDB2), an E3 ubiquitin ligase, as a pivotal regulator of lipid metabolism disorders in type II diabetes mellitus (T2DM). A mouse model of T2DM and primary mouse hepatocytes with steatosis were induced.
View Article and Find Full Text PDFGenes Dev
December 2024
Institute for Diabetes, Obesity, and Metabolism, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19146, USA;
The Cullin-3 E3 ligase adaptor protein SPOP targets proteins for ubiquitination and proteasomal degradation. We previously established the β-cell transcription factor (TF) and human diabetes gene PDX1 as an SPOP substrate, suggesting a functional role for SPOP in the β cell. Here, we generated a β-cell-specific deletion mouse strain ( ) and found that is necessary to prevent aberrant basal insulin secretion and for maintaining glucose-stimulated insulin secretion through impacts on glycolysis and glucose-stimulated calcium flux.
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