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Cellular and molecular mechanisms of kidney fibrosis

Sonja Djudjaj1, Peter Boor2

  • 1Institute of Pathology, RWTH University of Aachen, Germany.

Molecular Aspects of Medicine
|June 18, 2018
PubMed

Insights

Renal fibrosis, a key process in chronic kidney disease (CKD), involves excessive matrix deposition that impairs kidney function. This review details fibrosis in different kidney compartments and discusses anti-fibrotic treatment challenges.

Area of Science:

  • Nephrology
  • Pathology
  • Translational Medicine

Background:

  • Renal fibrosis is the common endpoint of chronic kidney injury and a primary driver of chronic kidney disease (CKD).
  • CKD affects over 10% of the global population, with limited therapeutic options.
  • Fibrosis leads to organ failure through excessive extracellular matrix deposition, disrupting kidney parenchyma.

Purpose of the Study:

  • To review the diverse manifestations, cellular origins, and key mediators of renal fibrosis across different kidney compartments.
  • To analyze the challenges in translating anti-fibrotic therapies into clinical practice.
  • To propose solutions and future research directions for combating renal fibrosis.

Main Methods:

  • Comprehensive literature review of renal fibrosis.
  • Analysis of histological compartments affected by fibrosis: glomeruli, tubulointerstitium, and vasculature.
  • Discussion of cellular origins and pathogenic processes.
  • Evaluation of clinical translation challenges for anti-fibrotic treatments.

Main Results:

  • Fibrosis presents differently in glomeruli (glomerulosclerosis), tubulointerstitium (interstitial fibrosis), and vasculature (arteriosclerosis, perivascular fibrosis).
  • Emerging mediators and cellular processes driving fibrosis in each compartment are identified.
  • Significant hurdles exist in translating experimental anti-fibrotic strategies to effective clinical treatments.

Conclusions:

  • Understanding the specific mechanisms of fibrosis in each kidney compartment is crucial.
  • Overcoming clinical translation barriers is essential for developing effective anti-fibrotic therapies.
  • Future research should focus on targeted interventions and innovative therapeutic strategies for CKD.
Keywords:
Animal modelsFibrogenesisFibrosisGlomerulosclerosisKidneyMicrovasculature

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