Modulation of glomerulosclerosis.
Regardless of the initial injury, the long-term consequence for the patient depends upon the ensuing balance of profibrotic vs reparative modulators activated. The glomerulus has some capacity for repair. Even when sclerosis has developed with accumulation of extracellular matrix, this lesion may be remodeled, with a change in balance between profibrotic and antifibrotic and collagen synthesis vs proteolytic mediators. We will focus here on the interplay between mediators of fibrosis and reparative mechanisms and potential regression of fibrosis. Based on the clinical efficacy of interventions that inhibit angiotensin, we will focus on factors related to the renin-angiotensin system.
Ma
Li-Jun
LJ
MCN C3310, Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Fogo
Agnes B
AB
D000809:Angiotensins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D003094:Collagen / Q000096:biosynthesis*; D005109:Extracellular Matrix / Q000378:metabolism* / Q000473:pathology; D005355:Fibrosis; D005923:Glomerulosclerosis, Focal Segmental / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D006801:Humans; D007678:Kidney Glomerulus / Q000378:metabolism* / Q000473:pathology; D012038:Regeneration; D012084:Renin-Angiotensin System; D012598:Sclerosis