Regulation of matrix synthesis, remodeling and accumulation in glomerulosclerosis.
After injury the body normally undergoes a repair process, however when this event becomes deregulated the pathological condition of fibrosis occurs. There are many similarities with respect to the fundamental mechanisms that regulate sclerosis in different organ systems. In this review we utilize the pathological entity of glomerulosclerosis in the kidney to highlight some of the general paradigms whereby extracellular matrix (ECM) is deposited in greater quantities than it is degraded. Our review discusses how genetic and structural abnormalities of specific ECM components can result in fibrosis. In addition, we outline how some key growth factors, integrins and oxidative stress play a role in the development of glomerulosclerosis.
Pozzi
Ambra
A
Department of Medicine, Division of Nephrology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA. ambra.pozzi@vanderbilt.edu
Voziyan
Paul A
PA
Hudson
Billy G
BG
Zent
Roy
R
D000818:Animals; D005109:Extracellular Matrix / Q000502:physiology*; D005923:Glomerulosclerosis, Focal Segmental / Q000378:metabolism / Q000473:pathology*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D016023:Integrins / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D007678:Kidney Glomerulus / Q000473:pathology / Q000648:ultrastructure; D018384:Oxidative Stress / Q000502:physiology; D050050:Protein Carbonylation / Q000502:physiology; D014157:Transcription Factors
D017127:Glycation End Products, Advanced; D016023:Integrins; D036341:Intercellular Signaling Peptides and Proteins; D014157:Transcription Factors