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One of the great challenges of lung transplantation is the development of progressive small airway fibrosis leading to pulmonary function decline and allograft loss. Termed as chronic lung allograft dysfunction (CLAD), it is the leading cause of shortened long-term survival among lung transplant recipients and estimated to affect at least half of all recipients within 5 years after transplant.1 Risk factors for CLAD include type of transplant (single vs bilateral), infections, gastro-oesophageal reflux, graft ischaemic time, ischaemia–reperfusion injury, air pollution exposure, acute cellular rejection (ACR) episodes and specific antibody development.2 In this issue of Thorax, Faust and colleagues propose a new risk factor for CLAD: short donor telomere length (TL).3
Telomeres consist of repetitive DNA sequences bound to shelterin protein complex at chromosome ends to provide protection from degradation during cell division. Short TL has been identified as a major contributor to lung disease, most notably as a genetic mediator of a subset of patients with idiopathic pulmonary fibrosis (IPF). In particular, mutations in multiple telomere-related genes that code for components of the telomerase enzyme complex are known to be associated with familial idiopathic interstitial pneumonia (IIP), as well as a smaller subset of patients with sporadic …
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