Abstract
Tubulointerstitial fibrosis is a chronic and progressive process affecting kidneys during aging and in chronic kidney disease (CKD), regardless of cause. CKD and renal fibrosis affect half of adults above age 70 and 10% of the world's population. Although no targeted therapy yet exists to slow renal fibrosis, a number of important recent advances have clarified the cellular and molecular mechanisms underlying the disease. In this review, I highlight these advances with a focus on cells and pathways that may be amenable to therapeutic targeting. I discuss pathologic changes regulating interstitial myofibroblast activation, including profibrotic and proinflammatory paracrine signals secreted by epithelial cells after either acute or chronic injury. I conclude by highlighting novel therapeutic targets and approaches with particular promise for development of new treatments for patients with fibrotic kidney disease.
| Original language | English |
|---|---|
| Pages (from-to) | 309-326 |
| Number of pages | 18 |
| Journal | Annual review of physiology |
| Volume | 80 |
| DOIs | |
| State | Published - Feb 10 2018 |
Keywords
- Dedifferentiation
- Fibrosis
- Mesenchymal stem cell
- Myofibroblast
- Pericyte
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