Abstract
The regulation of proliferation and cell death is vital for homeostasis, but the mechanisms that coordinately balances these two events in rheumatoid arthritis (RA) remains largely unknown. In RA, the synovial lining increases through enhanced proliferation, migration, and/or decreased cell death. The aberrant decrease in apoptosis or increased cell cycle activity of fibroblast-like or macrophage-like synoviocytes is responsible for the synovial hyperplasia and contributes to the destruction of cartilage and bone. Recently, numerous molecules that modulate apoptosis and cell cycle have been implicated to play a role in RA. This review will describe the current understanding of the molecular mechanisms that govern apoptosis and cell cycle and their relationship to RA pathogenesis.
Current Molecular Medicine
Title: Regulation of Apoptosis and Cell Cycle Activity in Rheumatoid Arthritis
Volume: 1 Issue: 5
Author(s): Harris Perlman, Lisa J. Pagliari and Michael V. Volin
Affiliation:
Abstract: The regulation of proliferation and cell death is vital for homeostasis, but the mechanisms that coordinately balances these two events in rheumatoid arthritis (RA) remains largely unknown. In RA, the synovial lining increases through enhanced proliferation, migration, and/or decreased cell death. The aberrant decrease in apoptosis or increased cell cycle activity of fibroblast-like or macrophage-like synoviocytes is responsible for the synovial hyperplasia and contributes to the destruction of cartilage and bone. Recently, numerous molecules that modulate apoptosis and cell cycle have been implicated to play a role in RA. This review will describe the current understanding of the molecular mechanisms that govern apoptosis and cell cycle and their relationship to RA pathogenesis.
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Cite this article as:
Harris Perlman , Lisa J. Pagliari and Michael V. Volin , Regulation of Apoptosis and Cell Cycle Activity in Rheumatoid Arthritis, Current Molecular Medicine 2001; 1 (5) . https://dx.doi.org/10.2174/1566524013363429
DOI https://dx.doi.org/10.2174/1566524013363429 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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