Smad3 Signatures in Renal Inflammation and Fibrosis

Renal inflammation and fibrosis are key pathological features of acute kidney injury (AKI) and chronic kidney disease (CKD). Smad3 is a critical mediator of TGF-beta signaling and plays a pathogenic role in both renal inflammation and fibrosis. Smad3 can be activated not only by TGF-beta 1 but also by many stress molecules including angiotensin II (Ang II), advanced end products (AGEs), and C-reactive protein (CRP) under disease conditions. In addition, Smad3 can interact with other signaling pathways, such as the ERK/p38 MAPK and NF -KB pathways, to mediate renal inflammation and fibrosis. Mechanistically, Smad3 transcriptionally regulates many downstream target genes including microRNAs and long non-coding RNAs to cause cell death, inflammation, and fibrosis. Thus, targeting Smad3 or its downstream genes specifically related to renal inflammation and fibrosis should provide a novel therapeutic strategy to combat kidney diseases.

Automated summary

Renal inflammation and fibrosis are important pathological features of kidney diseases. Smad3 is a critical mediator in TGF-beta signaling and plays a role in the development of inflammation and fibrosis in the kidney. Smad3 can be activated by various stress molecules and interact with other signaling pathways to mediate these processes. Targeting Smad3 and its downstream genes may provide a new therapeutic strategy for kidney diseases.