Crosstalk between tubular epithelial cells and glomerular endothelial cells in diabetic kidney disease

Abstract

In recent years, although the development of clinical therapy for diabetic kidney disease (DKD) has made great progress, the progression of DKD still cannot be controlled. Therefore, further study of the pathogenesis of DKD and improvements in DKD treatment are crucial for prognosis. Traditional studies have shown that podocyte injury plays an important role in this process. Recently, it has been found that glomerulotubular balance and tubuloglomerular feedback (TGF) may be involved in the progression of DKD. Glomerulotubular balance is the specific gravity absorption of the glomerular ultrafiltrate by the proximal tubules, which absorbs only 65% to 70% of the ultrafiltrate. This ensures that the urine volume will not change much regardless of whether the glomerular filtration rate (GFR) increases or decreases. TGF is one of the significant mechanisms of renal blood flow and self‐regulation of GFR, but how they participate in the development of DKD in the pathological state and the specific mechanism is not clear. Injury to tubular epithelial cells (TECs) is the key link in DKD. Additionally, injury to glomerular endothelial cells (GECs) plays a key role in the early occurrence and development of DKD. However, TECs and GECs are close to each other in anatomical position and can crosstalk with each other, which may affect the development of DKD. Therefore, the purpose of this review was to summarize the current knowledge on the crosstalk between TECs and GECs in the pathogenesis of DKD and to highlight specific clinical and potential therapeutic strategies.

Complement C5 activation promotes type 2 diabetic kidney disease via activating STAT3 pathway and disrupting the gut‐kidney axis

“…27 In line with these reports, we found that involved in the pathology of DKD. 31,32 Thus, future studies designed to determine whether complement activation also affects other renal cell types and to elucidate the crosstalk between these cells during DKD are needed.…”

“…Therefore, hyperactivation of complement C5 may contribute to the development and progression of diabetic glomerulosclerosis in T2DM. However, other types of renal cells, such as podocytes and tubular epithelial cells, are also involved in the pathology of DKD 31,32 . Thus, future studies designed to determine whether complement activation also affects other renal cell types and to elucidate the crosstalk between these cells during DKD are needed.…”

Liraglutide improves obesity‐induced renal injury by alleviating uncoupling of the glomerular VEGF–NO axis in obese mice

“…These cells, in intimate contact with blood, are more sensitive to changes in circulatory conditions. 25…”

GLP-1 Receptor Agonists in Diabetic Kidney Disease: From Clinical Outcomes to Mechanisms

“…DKD is associated with endothelial dysfunction (Chen et al, 2020). Endothelial GLP-1R has been shown to be involved in endothelial dysfunction in a mouse angiotensin II-induced hypertension model (Helmstadter et al, 2020).…”