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Inflammatory Crosstalk Between Type 2 Diabetes and Sarcopenia: Insights from In Silico Evaluation
Cristina Russo1, Maria Stella Valle2, Maria Teresa Cambria3
1Section of Pathology, Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, 95123 Catania, Italy.
International Journal of Molecular Sciences
|August 28, 2025
Summary
Mitochondrial dysfunction links sarcopenia and type 2 diabetes mellitus (T2DM). Key energy metabolism genes are downregulated, suggesting a shared molecular mechanism for these age-related conditions.
Area of Science:
- Gerontology
- Metabolic Diseases
- Molecular Biology
Background:
- Sarcopenia and type 2 diabetes mellitus (T2DM) are prevalent chronic conditions in the elderly.
- These conditions often coexist, but the underlying molecular mechanisms remain poorly understood.
- Sarcopenia, characterized by muscle mass and function loss, is common in T2DM patients.
Purpose of the Study:
- To investigate the shared molecular mechanisms between sarcopenia and T2DM.
- To identify potential biomarkers and therapeutic targets for both conditions.
Main Methods:
- Gene expression datasets were analyzed to identify differentially expressed genes (DEGs).
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed.
- Protein-protein interaction (PPI) networks were constructed to identify hub genes.
Main Results:
- Enrichment analyses highlighted mitochondrial function, oxidative phosphorylation, and immune-inflammatory responses.
- A PPI network identified a hub of five key genes in energy metabolism.
- Downregulation of these hub genes suggests mitochondrial dysfunction as a shared mechanism.
Conclusions:
- Mitochondrial dysfunction is a potential shared molecular mechanism underlying sarcopenia and T2DM.
- Identified hub genes may serve as biomarkers for both conditions.
- These findings offer insights for developing targeted therapies for metabolic disruption and muscle decline.
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