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Signaling Pathways Involved in Diabetic Renal Fibrosis
- Source :
- Frontiers in Cell and Developmental Biology, Vol 9 (2021), Frontiers in Cell and Developmental Biology
- Publication Year :
- 2021
- Publisher :
- Frontiers Media SA, 2021.
-
Abstract
- Diabetic kidney disease (DKD), as the most common complication of diabetes mellitus (DM), is the major cause of end-stage renal disease (ESRD). Renal interstitial fibrosis is a crucial metabolic change in the late stage of DKD, which is always considered to be complex and irreversible. In this review, we discuss the pathological mechanisms of diabetic renal fibrosis and discussed some signaling pathways that are closely related to it, such as the TGF-β, MAPK, Wnt/β-catenin, PI3K/Akt, JAK/STAT, and Notch pathways. The cross-talks among these pathways were then discussed to elucidate the complicated cascade behind the tubulointerstitial fibrosis. Finally, we summarized the new drugs with potential therapeutic effects on renal fibrosis and listed related clinical trials. The purpose of this review is to elucidate the mechanisms and related pathways of renal fibrosis in DKD and to provide novel therapeutic intervention insights for clinical research to delay the progression of renal fibrosis.
- Subjects :
- 0301 basic medicine
signaling pathway
TGF-β
QH301-705.5
Disease
Review
Bioinformatics
urologic and male genital diseases
03 medical and health sciences
Cell and Developmental Biology
0302 clinical medicine
Diabetes mellitus
Renal fibrosis
Medicine
Biology (General)
Protein kinase B
Pathological
PI3K/AKT/mTOR pathway
business.industry
Wnt signaling pathway
Cell Biology
medicine.disease
renal fibrosis
diabetic kidney disease
030104 developmental biology
030220 oncology & carcinogenesis
Tubulointerstitial fibrosis
cross-talk
business
Developmental Biology
Subjects
Details
- Language :
- English
- ISSN :
- 2296634X
- Volume :
- 9
- Database :
- OpenAIRE
- Journal :
- Frontiers in Cell and Developmental Biology
- Accession number :
- edsair.doi.dedup.....112ab0f9660ad88b38a462bfc41f3d1e
- Full Text :
- https://doi.org/10.3389/fcell.2021.696542