Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions
Cellular senescence, a phenomenon characterized by the accumulation of dysfunctional, metabolically active cells, is increasingly recognized to be a key player in aging-related metabolic disorders. It is accelerated by hyperglycemia through various molecular pathways, positioning it as a critical me...
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MDPI AG
2025-06-01
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| Series: | Diabetology |
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| Online Access: | https://www.mdpi.com/2673-4540/6/6/48 |
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| author | Selene Sodini Milton Fabián Suarez-Ortegón |
| author_facet | Selene Sodini Milton Fabián Suarez-Ortegón |
| author_sort | Selene Sodini |
| collection | DOAJ |
| description | Cellular senescence, a phenomenon characterized by the accumulation of dysfunctional, metabolically active cells, is increasingly recognized to be a key player in aging-related metabolic disorders. It is accelerated by hyperglycemia through various molecular pathways, positioning it as a critical mechanism in the pathophysiology of type 2 diabetes mellitus (T2D) and a potential therapeutic target. Emerging evidence from animal and clinical studies suggests that the usage of senolytic drugs, which selectively deplete senescent cells, can improve blood glucose regulation and mitigate diabetic complications. However, despite the conceptual feasibility of this approach, several challenges remain in their translation to the clinic: the molecular mechanisms underlying the pathogenicity of cellular senescence in vivo remain incompletely understood, and organ-specific effects of senolytic administration are yet to be fully elucidated to ensure their safety and efficacy in clinical applications. This review explores the characteristics of cellular senescence and the senescence-associated secretory phenotype (SASP) in key tissues involved in glucose homeostasis, including the pancreas, liver, adipose tissue, and skeletal muscle and the potential applications of targeting cellular senescence as a therapeutic strategy for T2D management. |
| format | Article |
| id | doaj-art-4ab7b1b93695451e9f4a97f923965604 |
| institution | Kabale University |
| issn | 2673-4540 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Diabetology |
| spelling | doaj-art-4ab7b1b93695451e9f4a97f9239656042025-08-20T03:27:28ZengMDPI AGDiabetology2673-45402025-06-01664810.3390/diabetology6060048Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future DirectionsSelene Sodini0Milton Fabián Suarez-Ortegón1Department of Laboratory Medicine, Faculty of Medicine, Lund University, 222 62 Lund, SwedenDepartment of Food and Nutrition, Faculty of Health Sciences, Pontificia Universidad Javeriana Seccional Cali, Cali 760031, ColombiaCellular senescence, a phenomenon characterized by the accumulation of dysfunctional, metabolically active cells, is increasingly recognized to be a key player in aging-related metabolic disorders. It is accelerated by hyperglycemia through various molecular pathways, positioning it as a critical mechanism in the pathophysiology of type 2 diabetes mellitus (T2D) and a potential therapeutic target. Emerging evidence from animal and clinical studies suggests that the usage of senolytic drugs, which selectively deplete senescent cells, can improve blood glucose regulation and mitigate diabetic complications. However, despite the conceptual feasibility of this approach, several challenges remain in their translation to the clinic: the molecular mechanisms underlying the pathogenicity of cellular senescence in vivo remain incompletely understood, and organ-specific effects of senolytic administration are yet to be fully elucidated to ensure their safety and efficacy in clinical applications. This review explores the characteristics of cellular senescence and the senescence-associated secretory phenotype (SASP) in key tissues involved in glucose homeostasis, including the pancreas, liver, adipose tissue, and skeletal muscle and the potential applications of targeting cellular senescence as a therapeutic strategy for T2D management.https://www.mdpi.com/2673-4540/6/6/48agingdiabetes mellitus type 2insulin-secreting cellssenolyticssenomorphicscellular senescence |
| spellingShingle | Selene Sodini Milton Fabián Suarez-Ortegón Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions Diabetology aging diabetes mellitus type 2 insulin-secreting cells senolytics senomorphics cellular senescence |
| title | Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions |
| title_full | Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions |
| title_fullStr | Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions |
| title_full_unstemmed | Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions |
| title_short | Senolytic Interventions for Type 2 Diabetes: Current Evidence and Future Directions |
| title_sort | senolytic interventions for type 2 diabetes current evidence and future directions |
| topic | aging diabetes mellitus type 2 insulin-secreting cells senolytics senomorphics cellular senescence |
| url | https://www.mdpi.com/2673-4540/6/6/48 |
| work_keys_str_mv | AT selenesodini senolyticinterventionsfortype2diabetescurrentevidenceandfuturedirections AT miltonfabiansuarezortegon senolyticinterventionsfortype2diabetescurrentevidenceandfuturedirections |