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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
1995-11-21
|
| pubmed:abstractText |
Renal epithelial cells that are part of an intact tubule epithelium divide at a very slow rate. However, in response to physiological signals or pathological processes, their rate of growth can rapidly increase. In these situations, the growth response can be hyperplasic (an increase in cell number) and/or hypertrophic (an increase in cell size). This article reviews our current understanding of the signaling pathways involved in renal epithelial cell hyperplasia and hypertrophy. Hyperplasia involves an initiating mitogenic stimulus, followed by the synthesis of a number of proteins that regulate a cascade of events governing progression through each of the phases of the cell cycle (G1, S, G2, and M phases). Renal epithelial cell hypertrophy can occur by cell cycle-dependent or -independent mechanisms. Cell cycle-dependent hypertrophy involves signals that cause cells to enter the first phase of the cell cycle (G1), but become arrested before leaving this phase. The consequence of these two sequential events is cell growth without DNA replication and, thus, cell hypertrophy. pRB plays a key role is the development of this form of hypertrophy. Cell cycle-independent hypertrophy probably involves inhibition of pH-sensitive lysosomal enzymes, leading to decreased protein degradation, and consequently an increase in cell protein content and cell hypertrophy.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0270-9295
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
15
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
327-40
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading | |
| pubmed:year |
1995
|
| pubmed:articleTitle |
Renal epithelial cell hyperplasia and hypertrophy.
|
| pubmed:affiliation |
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8856, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
|