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Isolation of Valvular Endothelial Cells
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Role of Endothelial Cells in Renal Fibrosis

Zhen Yang1, Li-Jie He1, Shi-Ren Sun2

  • 1Department of Nephrology, The First Affiliated Hospital of Air Force Medical University, Xi'an, Shaanxi, China.

Advances in Experimental Medicine and Biology
|August 11, 2019
PubMed

Insights

Endothelial cells (ECs) play a crucial role in kidney fibrosis, a common cause of kidney failure. New research highlights endothelial-to-mesenchymal transition (EndMT) and dysfunction as key drivers of fibrosis progression.

Area of Science:

  • Nephrology
  • Cell Biology
  • Pathophysiology

Background:

  • Renal fibrosis is a major pathway to end-stage renal failure.
  • Understanding its mechanisms is key for treating chronic kidney diseases.
  • Current focus is on tubular cells, interstitial cells, inflammation, and ECM homeostasis.

Purpose of the Study:

  • To interpret the role of endothelial cells (ECs) in renal fibrosis.
  • To analyze molecular pathways of endothelial-to-mesenchymal transition (EndMT) in fibrosis.
  • To investigate EndMT-independent endothelial dysfunction in renal fibrosis.

Main Methods:

  • Review of emerging studies on endothelial cell involvement in renal fibrosis.
  • Analysis of molecular mechanisms and signaling pathways.
  • Examination of both EndMT-dependent and independent endothelial dysfunction.

Main Results:

  • Endothelial cells contribute to renal fibrosis through EndMT and dysfunction.
  • These processes accelerate fibrosis and myofibroblast proliferation.
  • Specific molecules and pathways driving these changes are identified.

Conclusions:

  • Endothelial cell dysfunction is a significant, newly recognized mechanism in renal fibrosis.
  • Targeting ECs and their pathways offers potential therapeutic strategies for kidney disease.
  • Further research into EndMT and endothelial dysfunction is warranted.
Keywords:
EndMTEndothelial cellEndothelial dysfunctionRenal fibrosis

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