Molecular mechanisms of renal hypertrophy: role of p27Kip1

Kidney Int. 1999 Oct;56(4):1262-5. doi: 10.1046/j.1523-1755.1999.00695.x.


There are two fundamentally different growth responses for cells comprising the nephron: hyperplasia or hypertrophy. Cells that progress through the normal cell cycle double their DNA content and eventually divide during mitosis. Those cells that hypertrophy stop the growth process in the G1-phase of the cell cycle; while they increase in size, protein and RNA content, they cannot duplicate their set of chromosomes because they never pass through the S-phase of the cell cycle. Hypertrophy may be an early compensatory mechanism to initially replace the loss of functioning tissue, however, this maladaptive process eventually fosters progressive loss of renal function. Since progression of the cell through the G1 to S-phases is regulated by cyclins D, E and A, which in turn bind and activate cyclin dependent kinases (CDKs), evidence has been accumulating on a particular CDK-inhibitor protein, p27Kip1, which is speculated to be a key to the complex process of the G1/S cell cycle transition. This article examines the mechanisms of the proliferative growth response following acute tubular necrosis, and compensatory hypertrophy of glomerular and tubule cells, with a particular focus on the protein p27Kip1.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Cycle Proteins*
  • Cell Division / physiology
  • Cyclin-Dependent Kinase Inhibitor p27
  • Humans
  • Hypertrophy
  • Kidney Glomerulus / pathology*
  • Kidney Tubular Necrosis, Acute / pathology*
  • Kidney Tubules / pathology*
  • Microtubule-Associated Proteins / physiology*
  • Tumor Suppressor Proteins*


  • Cell Cycle Proteins
  • Microtubule-Associated Proteins
  • Tumor Suppressor Proteins
  • Cyclin-Dependent Kinase Inhibitor p27