The potential role of inflammatory and fibrogenic cytokines in the glomerular diseases

J Lipid Mediat Cell Signal. 1994 Feb;9(1):55-74.

Abstract

In recent years increasing evidence has been accumulated on the role of cytokines in mediating glomerular and renal damage. Many such cytokines are released in the inflamed glomeruli by leukocytes and intrinsic glomerular cells. Cytokines not only recruit inflammatory cells into the injured glomeruli, but also induce a variety of responses on glomerular cells that range from a direct toxic effect to shape changes, proliferation, and induction of the release of inflammatory mediators and extracellular matrix, and could promote further glomerular damage. Moreover, exogenous administration of cytokines has induced glomerular injury in healthy animals and has enhanced renal damage in animals with glomerulonephritis. Anti-cytokine strategies have proved to be effective therapeutical alternatives in experimental models of glomerular diseases and may provide a more specific approach to the management of human glomerulonephritis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cytokines / biosynthesis
  • Cytokines / physiology*
  • Glomerular Mesangium / immunology
  • Glomerular Mesangium / metabolism
  • Glomerulonephritis / immunology
  • Glomerulonephritis / physiopathology*
  • Glomerulonephritis / therapy
  • Humans
  • Inflammation
  • Interleukin-1 / pharmacology
  • Interleukin-1 / physiology
  • Interleukin-6 / pharmacology
  • Interleukin-6 / physiology
  • Kidney Glomerulus / drug effects
  • Kidney Glomerulus / physiology*
  • Kidney Glomerulus / physiopathology
  • Platelet-Derived Growth Factor / pharmacology
  • Platelet-Derived Growth Factor / physiology
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta / physiology
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / pharmacology
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Platelet-Derived Growth Factor
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha