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[Fibrinolytic factors: novel molecular targets for cytokine storm-associated diseases]

Koichi Hattori1,2, Hiroshi Shimazu3, Satoshi Takahashi4

  • 1Center for Genomic & Regenerative Medicine, Juntendo University Graduate School of Medicine.

[Rinsho Ketsueki] the Japanese Journal of Clinical Hematology
|June 6, 2022
PubMed

Insights

Understanding the cytokine storm in severe COVID-19 reveals the fibrinolytic system

Area of Science:

  • Immunology
  • Pathophysiology
  • Vascular Biology

Background:

  • The severe coronavirus disease 2019 (COVID-19) has caused millions of deaths globally.
  • The "cytokine storm," driven by the coagulation/fibrinolytic system, significantly contributes to COVID-19 pathology.
  • Endothelial cells play a crucial role in modulating inflammatory and coagulation factors.

Purpose of the Study:

  • To elucidate the role of the fibrinolytic system in inflammatory diseases, particularly COVID-19.
  • To explore potential therapeutic targets within the angiocrine and fibrinolytic systems for managing inflammatory conditions.

Main Methods:

  • Review of existing research on the pathophysiology of COVID-19.
  • Focus on the mechanisms of the cytokine storm and vascular endothelial damage.
  • Analysis of the fibrinolytic system's involvement in inflammatory disease progression.

Main Results:

  • The coagulation/fibrinolytic system is central to the "cytokine storm" observed in severe COVID-19.
  • Vascular endothelial damage destabilizes the angiocrine system, exacerbating inflammation.
  • Imbalanced angiocrine factors and cytokines are key contributors to COVID-19 complications.

Conclusions:

  • The fibrinolytic system is a significant factor in the pathophysiology of inflammatory diseases like COVID-19.
  • Targeting angiocrine and fibrinolytic factors presents a promising avenue for novel therapeutic strategies.
  • Further research into these pathways could lead to effective treatments for severe COVID-19 and related inflammatory conditions.

Keywords:
Angiocrine factorsEndotheliumInflammationMatrix metalloproteinases

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