Unveiling the immune microenvironment in diabetic nephropathy: from mechanisms to therapeutics

TL;DR

This paper explores how immune factors contribute to diabetic kidney disease and suggests new diagnostic and treatment approaches.

Contribution

It systematically reviews the immune microenvironment's role in diabetic nephropathy and proposes precision medicine strategies.

Findings

The immune microenvironment, including immune cells and cytokines, drives diabetic nephropathy progression.

Immune cell interactions with kidney cells and gut microbiota-immune axes are key mechanisms in disease development.

Potential immune-related biomarkers and therapies are identified for precision medicine in diabetic nephropathy.

Abstract

Diabetic nephropathy (DN) is one of the most common microvascular complications of diabetes and is the primary cause of end-stage renal disease, imposing a significant burden on patients’ health, the medical and economic systems. The traditional view holds that the pathogenesis of DN is mainly related to metabolic disorders caused by hyperglycemia, genetic susceptibility, and abnormal hemorheology. However, with the deep integration of immunology and nephrology research, more and more evidence indicates that immune factors play a core role in its pathogenesis. The renal immune microenvironment is a network composed of immune cells, cytokines, and matrix components, which promotes the progression of the disease through continuous inflammation, immune cell infiltration, and imbalanced homeostasis. This study systematically reviews the core mechanisms of the immune microenvironment in the occurrence and development of DN, focusing on the interaction between immune cells and innate renal cells, as well as the regulatory roles of the intestinal microbiota and immune axes. We also summarize possible diagnostic markers and treatment strategies related to immunity, aiming to provide new ideas for precision medicine of DN.

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