Cellular and molecular mediators in common pathway mechanisms of chronic renal disease progression.
Injury mechanisms activated by the hemodynamic adaptations to nephron loss are considered to represent a final common pathway that underlies the progressive nature of chronic renal disease. In this article, we review experimental evidence that the induction of cell adhesion molecule, cytokine and profibrotic growth factor gene expression and the resultant renal infiltration by inflammatory cells, especially macrophages, are important components of these common pathway mechanisms. Interventions aimed at inhibiting these mechanisms may offer new treatments for slowing or arresting the progression of chronic renal disease.
Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. mtaal@rics.bwh.harvard.edu
M W
MW
Taal
S A
SA
Omer
M K
MK
Nadim
H S
HS
Mackenzie
D000818:Animals; D015815:Cell Adhesion Molecules / Q000502:physiology; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology; D018450:Disease Progression; D006133:Growth Substances / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D007674:Kidney Diseases / Q000503:physiopathology* / Q000628:therapy
D015815:Cell Adhesion Molecules; D016207:Cytokines; D006133:Growth Substances