Molecular heterogeneity in type 2 diabetes: implications for kidney disease

Abstract

The findings presented throughout this thesis underscore the importance of moving beyond a one-size-fits-all view of type 2 diabetes. Together, they show that type 2 diabetes should not be viewed as a single, homogeneous disease, but rather as a highly heterogeneous condition driven by underlying molecular diversity. This heterogeneity is evident across multiple biological layers, including gene expression, non-coding RNAs, metabolites, and tissue-specific regulatory networks.

Importantly, this molecular variability also contributes to differences in susceptibility to and progression of complications such as diabetic kidney disease (DKD). Specific molecular signatures appear to influence individual risk profiles, suggesting that patients with type 2 diabetes may differ substantially at a biological level in ways that are clinically relevant.

Together, these findings highlight the importance of a precision medicine approach to type 2 diabetes. Rather than applying uniform treatment strategies, future research and clinical practice should account for this biological diversity, aim to understand its underlying mechanisms, and translate these insights into targeted interventions. Overall, the work emphasizes that both type 2 diabetes and its complications can only be fully understood through an integrated, multi-layered biological perspective.