The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy

Abstract

Diabetic nephropathy (DN) is a common complication affecting many diabetic patients, leading to end-stage renal disease. However, its pathogenesis still needs to be fully understood to enhance the effectiveness of treatment methods. Traditional theories are predominantly centered on glomerular injuries and need more explicit explanations of recent clinical observations suggesting that renal tubules equally contribute to renal function and that tubular lesions are early features of DN, even occurring before glomerular lesions. Although the conventional view is that DN is not an inflammatory disease, recent studies indicate that systemic and local inflammation, including tubulointerstitial inflammation, contributes to the development of DN. In patients with DN, intrinsic tubulointerstitial cells produce many proinflammatory factors, leading to medullary inflammatory cell infiltration and activation of inflammatory cells in the interstitial region. Therefore, understanding the molecular mechanism of renal tubulointerstitial inflammation contributing to DN injury is of great significance and will help further identify key factors regulating renal tubulointerstitial inflammation in the high glucose environment. This will aid in developing new targets for DN diagnosis and treatment and expanding new DN treatment methods.

Keywords:

• diabetic nephropathy
• renal tubules
• renal tubular injury
• renal tubulointerstitial inflammation
• DN injury

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis, and interpretation, or in all these areas; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that there is no conflict of interest regarding the publication of this paper.

Additional information

Funding

This work was supported by the 2022 Health Sciences and Technology program of Hangzhou: General Project Category A (No. A20220084) and the Biomedical and Health Industry Development Support Science and Technology Project in Hangzhou (No.2022WJC064). This work was also supported by a grant RO1DK118017 (PCS) from the National Institutes of Health, Bethesda, MD, USA.