New insights into the role of immunity and inflammation in diabetic kidney disease in the omics era

Front Immunol. 2024 Feb 29:15:1342837. doi: 10.3389/fimmu.2024.1342837. eCollection 2024.

Abstract

Diabetic kidney disease (DKD) is becoming the leading cause of chronic kidney disease, especially in the industrialized world. Despite mounting evidence has demonstrated that immunity and inflammation are highly involved in the pathogenesis and progression of DKD, the underlying mechanisms remain incompletely understood. Substantial molecules, signaling pathways, and cell types participate in DKD inflammation, by integrating into a complex regulatory network. Most of the studies have focused on individual components, without presenting their importance in the global or system-based processes, which largely hinders clinical translation. Besides, conventional technologies failed to monitor the different behaviors of resident renal cells and immune cells, making it difficult to understand their contributions to inflammation in DKD. Recently, the advancement of omics technologies including genomics, epigenomics, transcriptomics, proteomics, and metabolomics has revolutionized biomedical research, which allows an unbiased global analysis of changes in DNA, RNA, proteins, and metabolites in disease settings, even at single-cell and spatial resolutions. They help us to identify critical regulators of inflammation processes and provide an overview of cell heterogeneity in DKD. This review aims to summarize the application of multiple omics in the field of DKD and emphasize the latest evidence on the interplay of inflammation and DKD revealed by these technologies, which will provide new insights into the role of inflammation in the pathogenesis of DKD and lead to the development of novel therapeutic approaches and diagnostic biomarkers.

Keywords: diabetic kidney disease; epigenomics; genomics; inflammation; metabolomics; proteomics; transcriptomics.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Diabetes Mellitus* / metabolism
  • Diabetic Nephropathies* / pathology
  • Genomics
  • Humans
  • Inflammation / metabolism
  • Kidney / pathology
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / genetics

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Natural Science Foundation of China [82270764, 82022009 to YZ], Guangdong Special Support Program [2017TQ04R549 to YZ], Key Laboratory of National Health Commission [2002B60118], and Guangdong Provincial Key Laboratory of Nephrology [2020B1212060028].