Published online Mar 28, 2015. doi: 10.5320/wjr.v5.i1.40
Peer-review started: September 26, 2014
First decision: November 19, 2014
Revised: December 6, 2014
Accepted: December 18, 2014
Article in press: December 20, 2014
Published online: March 28, 2015
Processing time: 180 Days and 3.4 Hours
The tumor suppressor gene p53 regulates a wide range of cellular processes including cell cycle progression, proliferation, apoptosis and tissue development and remodeling. Lung cell apoptosis and tissue remodeling have critical roles in many lung diseases. Abnormal proliferation or resistance to apoptosis of lung cells will lead to structural changes of many lung tissues, including the pulmonary vascular wall, small airways and lung parenchyma. Among the many lung diseases caused by vascular cell apoptosis and tissue remodeling are chronic obstructive pulmonary disease, bronchial asthma and pulmonary arterial hypertension. Recent advances in biology and medicine have provided new insights and have resulted in new therapeutic strategies for tissue remodeling in human and animal models. This review is focused on lung disease susceptibility associated with the p53 pathway and describes molecular mechanisms upstream and downstream of p53 in lung tissue remodeling. Improved understanding of structural changes associated with pulmonary vascular remodeling and lung cell apoptosis induced by the p53 pathway may new provide therapeutic targets.
Core tip: The activated p53 protein and its associated pathway play a pivotal role in tissue remodeling in chronic obstructive pulmonary disease, asthma and pulmonary hypertension. p53 protein regulates numerous genes and proteins associated with cell cycle arrest and apoptosis. In response to oxidative stress or hypoxia, p53 can become stabilized and activate signal transduction towards lung tissue remodeling and functional loss.