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Annual Review of Physiology· 2017Q1· Review

Mechanisms of Renal Fibrosis

Benjamin D. Humphreys

Short summary

Recent advances clarify cellular and molecular mechanisms of tubulointerstitial fibrosis, a progressive kidney disease affecting 10% of the world's population and half of adults over 70.

AI-generated from the title and abstract; the full text is not read.

Key points

  • Tubulointerstitial fibrosis is a chronic, progressive kidney disease associated with aging and CKD.
  • It affects a significant portion of the global population, particularly older adults.
  • Recent research has elucidated cellular and molecular mechanisms driving fibrosis.
  • Specific pathways involving epithelial cell-derived signals and myofibroblast activation are central to the disease process.

AI-generated from the title and abstract; the full text is not read.

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.

The authors' abstract, as published at the source. Annual Review of Physiology, 2017 · DOI ↗

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Field: Nephrology

NephrologyMedicine