Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation

These findings elucidated the involvement of the TLR4/MyD88/PKCδ/SHP-1 signaling cascade in diabetic podocyte injury and inflammation, provided evidence for the renal protective and therapeutic potential of podocyte-specific targeting TLR4 in the challenge of DKD and might shed light on therapeutic strategies in proteinuric diseases.