Relaxin regulates collagen overproduction associated with experimental progressive renal fibrosis.
Progressive fibrosis due to excess extracellular matrix (primarily collagen) is the final common pathway in all forms of chronic renal disease, regardless of etiology, and leads to tissue dysfunction, when normal tissue is replaced by scar tissue. Emerging work from ourselves and others suggests that the naturally occurring hormone relaxin has the potential to limit renal collagen production and reorganization, while increasing its degradation. The outlined studies demonstrate relaxin's potential as an antifibrotic agent against experimental progressive renal disease.
Samuel
Chrishan S
CS
Howard Florey Institute of Experimental Physiology & Medicine, University of Melbourne, Parkville, Victoria 3010, Australia. c.samuel@hfi.unimelb.edu.au
Mookerjee
Ishanee
I
Masterson
Rosemary
R
Tregear
Geoffrey W
GW
Hewitson
Tim D
TD
D000375:Aging / Q000502:physiology; D000818:Animals; D002478:Cells, Cultured; D003094:Collagen / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D018450:Disease Progression; D005260:Female; D005347:Fibroblasts; D005355:Fibrosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D007674:Kidney Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D051379:Mice; D051381:Rats; D012065:Relaxin / Q000172:deficiency / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology*
D012065:Relaxin; D003094:Collagen