PURPOSE OF REVIEW: @entity740 are emerging as a worldwide public health problem. Clarification of the mechanisms underlying progression of proteinuric @entity8 received significant input from the generation of transgenic and knockout animals and from novel approaches to block mediators of injury. Reviewed here are advances in animal models used as a tool to address some relevant questions to the pathophysiology of @entity1 chronic @entity8 . RECENT FINDINGS: Gene targeting in rodents identified podocyte loss as central event in the development of @entity631 . The trigger is dysfunction or absence of podocyte molecules that stabilize the slit diaphragm or anchor foot processes to the basement membrane. Sustained injury of the glomerular barrier to proteins is transmitted to the tubulointerstitial compartment leading to @entity32 and @entity82 . Blocking NF-kappaB activity and chemokine signals in the kidney effectively interrupts such process. Growth factors produced by tubular cells and inflammatory cells contribute to interstitial fibrogenesis via myofibroblast activation. SUMMARY: Development of genetically engineered animals and techniques to specifically manipulate cellular mediators has highlighted the determinants of @entity631 and @entity130 . This knowledge will provide basis for novel interventions to protect the podocyte in chronic progressive glomerulopathies and to halt @entity8 and loss of function.

Progression of XXXX : insights from animal models.

@entity1 :: ('9606', 'Species') :: ['human'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity8 :: ('MESH:D007674', 'Disease') :: ['nephropathies', 'renal scarring'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity740 :: ('MESH:D051436', 'Disease') :: ['Chronic kidney diseases'] @entity631 :: ('MESH:D005921', 'Disease') :: ['glomerulosclerosis'] @entity130 :: ('MESH:D014947', 'Disease') :: ['tubulointerstitial injury']
@entity740 :: (MESH:D051436,Disease) :: ['chronic kidney disease']
