Autophagy is a highly conserved and tightly regulated cellular process involved in the turnover of cytoplasmic organelles and proteins through a lysosome-dependent degradation process. The aim of this project is to understand the role of autophagy in the development of idiopathic pulmonary fibrosis (IPF), a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause.
Idiopathic pulmonary fibrosis (IPF) is a life threatening condition of the lungs where tissue becomes thickened, stiff, and scarred due to an unknown cause, which limits the amount of oxygen that gets into the blood. With less oxygen in the blood, IPF patients can get breathlessness from everyday activities like walking. Latest research suggests about 6,000 people are diagnosed with IPF every year in the UK. At the moment, there is no cure available for the disease and a better understanding of how it develops is therefore urgently needed to help us find more effective, long-lasting treatments.
In this project, we will look at a body mechanism called ‘autophagy’ (from the Greek for ‘self-eating’) and its potential link to the development of IPF: a healthy cell performs an ongoing clean-up process to keep functioning normally, by digesting built-up internal structures. In patients suffering from IPF, previously healthy cells become damaged through scar tissue, and we believe that this could be due to the healthy cells losing their ability to ‘self-eat’. In our research, we will test this theory by developing a 3-dimensional cellular model of IPF to get a better understanding how the disease develops.
The results of the project will help us inform further research and new treatments for sufferers to reduce symptoms of this devastating disease and improve their quality of life.
Principal Investigators:
Dr Yihua Wang
,
Dr Rob Ewing
,
Prof Donna Davies
& Mark Jones
Funding:
Asthma Allergy & Inflammation Research Trust
&
The Institute for Life Science (IfLS)
Funding Duration:
January 2018-January 2021
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