TGF-beta and glomerulonephritis: anti-inflammatory versus prosclerotic actions.
TGF-beta has been considered as the key regulator in the generation of glomerulosclerosis. Despite abundant descriptive data, it still remains undetermined whether sustained, local expression of TGF-beta leads to irreversible glomerulosclerosis. There is no doubt that TGF-beta stimulates ECM production in the glomerulus, but this molecule has several anti-inflammatory properties as well. Towards a better understanding of the pathogenesis of glomerulonephritis and for the development of novel and efficient therapeutic interventions, extensive efforts should be made to clarify the 'bright side' of TGF-beta as well as its 'dark side' in individual experimental and human diseases, focusing especially on the concentration and the time-point at which its anti-inflammatory properties spill over into its prosclerotic actions.
Kitamura
M
M
Department of Medicine, University College London Medical School, UK.
Sütö
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D000818:Animals; D000893:Anti-Inflammatory Agents / Q000378:metabolism; D017209:Apoptosis; D002455:Cell Division; D016207:Cytokines / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D005355:Fibrosis; D005921:Glomerulonephritis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007678:Kidney Glomerulus / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D008264:Macrophages / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000502:physiology*
D000893:Anti-Inflammatory Agents; D016207:Cytokines; D016212:Transforming Growth Factor beta