作者: C. von Toerne , J. Bedke , S. Safi , S. Porubsky , N. Gretz
DOI: 10.1111/J.1600-6143.2011.03776.X
关键词:
摘要: Chronic renal allograft damage (CAD) is manifested by a smoldering inflammatory process that leads to transplant glomerulopathy, diffuse interstitial fibrosis and tubular atrophy with loss of structures. Using Fischer 344 (RT1lvl) Lewis (RT1l) rat model, transcriptomic profiling pathway mapping, we have previously shown dynamic dysregulation the Wnt signaling pathways may underlie progressive CAD. Retinoic acid, an important regulator differentiation during vertebrate embryogenesis, can moderate observed in this experimental model We show here subsets Hedgehog (Hh) canonical are linked pathophysiology fibrosis, cilia epithelia chronic dysfunction. Oral treatment 13cis retinoic acid (13cRA) was found selectively ameliorate Hh associated CAD, lead general preservation cilial Interplay between these helps explain therapeutic effects suggests future targets for moderating fibrosing organ damage.