Altered growth of renal cells is one of the early abnormalities detected after the onset of @entity6 . Cell culture studies whereby renal cells are exposed to high @entity413 concentrations have provided a considerable amount of insight into mechanisms of growth. In the glomerular compartment, there is a very early and self-limited proliferation of mesangial cells with subsequent @entity1184 , whereas proximal tubular cells primarily undergo @entity1184 . There is overwhelming evidence from in vivo and cell culture studies that induction of the @entity2533 ( @entity2533 ) system mediates the actions of high ambient @entity413 and that this system is pivotal for the @entity1184 of mesangial and tubular cells. Other factors such as hemodynamic forces, protein glycation products, and several mediators (for example, @entity2178 , @entity2232 , @entity2871 , and platelet-derived growth factor) may further amplify the synthesis of @entity2533 and/or the expression of its receptors in the @entity6 state. @entity1184 can be characterized by cell cycle arrest in the G1 phase. The molecular mechanism arresting mesangial cells in the G1 phase of the cell cycle is the induction of @entity1364 -dependent kinase (CdK) inhibitors such as @entity13525 and @entity994 , which bind to and inactivate @entity1364 -CdK complexes responsible for G1-phase exit. High- @entity413 -induced activation of protein kinase C and stimulated @entity2533 expression appear to be essential for stimulated expression of @entity13525 . In addition, a decreased turnover of protein caused by the inhibition of proteases contributes to @entity1184 . The development of irreversible renal changes in @entity6 such as @entity631 and tubulointerstitial @entity82 is always preceded by the early @entity1184 processes in the glomerular and the tubular compartments. It may still be debated whether @entity2316 will inevitably lead to irreversible fibrotic changes in the absence of other factors such as altered intraglomerular hemodynamics and genetic predisposition. Nevertheless, understanding cellular growth on a molecular level may help design a novel therapeutic approach to prevent or treat @entity2316 effectively.

Molecular mechanisms of XXXX .

@entity2871 :: ('CHEBI:26995', 'Chemical') :: ['thromboxane'] @entity1364 :: ('5111', 'Gene') :: ['cyclin'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetic', 'diabetes', 'diabetes mellitus'] @entity2232 :: ('1906', 'Gene') :: ['endothelin-1'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophy', 'hypertrophic', 'Cellular hypertrophy'] @entity2178 :: ('183', 'Gene') :: ['angiotensin II'] @entity2316 :: ('MESH:D003928', 'Disease') :: ['diabetic nephropathy', 'diabetic renal hypertrophy'] @entity2533 :: ('7040', 'Gene') :: ['TGF-beta', 'transforming growth factor-beta'] @entity13525 :: ('1027', 'Gene') :: ['p27Kip1'] @entity631 :: ('MESH:D005921', 'Disease') :: ['glomerulosclerosis'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose'] @entity994 :: ('1026', 'Gene') :: ['p21']
@entity2316 :: (MESH:D003928,Disease) :: ['diabetic renal hypertrophy']
