scholarly journals Lung Transplantation in Idiopathic Pulmonary Fibrosis

2018 ◽  
Vol 6 (3) ◽  
pp. 68 ◽  
Author(s):  
Rosalía Laporta Hernandez ◽  
Myriam Aguilar Perez ◽  
María Lázaro Carrasco ◽  
Piedad Ussetti Gil
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Transplantation ◽  
Immunosuppressive Treatment ◽  
Optimal Level ◽  
Waiting List ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Specific Patient ◽  
Post Transplant

Despite the advances in recent years in the treatment of idiopathic pulmonary fibrosis (IPF), it continues to be a progressive disease with poor prognosis. In selected patients, lung transplantation may be a treatment option, with optimal results in survival and quality of life. Currently, pulmonary fibrosis is the main cause of lung transplantation. However, mortality on the waiting list of these patients is high, since many patients are referred to the transplant units with advanced disease. There is not a parameter that can predict the survival of a specific patient. Different variables are to be considered in order to decide the right time to send them to a transplant unit. It is also very difficult to decide when to include these patients on the waiting list. Every patient diagnosed with IPF, without contraindications for surgery, should be referred early to a transplant unit for assessment. A uni or bilateral transplantation will be decided based on the characteristics of the patient and the experience of each center. The post-transplant survival of recipients with IPF is lower than that observed in other diseases, such as cystic fibrosis or chronic obstructive pulmonary disease as a consequence of their older age and the frequent presence of associated comorbidity. Post-transplant follow-up must be tight in order to assure optimal level of immunosuppressive treatment, detect complications associated with it, and avoid graft rejection. The main cause of long-term mortality is late graft dysfunction as a consequence of chronic rejection. Other complications, such as infections and tumors, must be considered.

scholarly journals Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 7 ◽  
Author(s):  
Norihito Omote ◽  
Maor Sauler
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Cell Fate ◽  
Cellular Senescence ◽  
Cellular Stress ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Non Coding Rnas

Cellular senescence is a cell fate implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Cellular senescence occurs in response to cellular stressors such as oxidative stress, DNA damage, telomere shortening, and mitochondrial dysfunction. Whether these stresses induce cellular senescence or an alternative cell fate depends on the type and magnitude of cellular stress, but also on intrinsic factors regulating the cellular stress response. Non-coding RNAs, including both microRNAs and long non-coding RNAs, are key regulators of cellular stress responses and susceptibility to cellular senescence. In this review, we will discuss cellular mechanisms that contribute to senescence in IPF and COPD and highlight recent advances in our understanding of how these processes are influenced by non-coding RNAs. We will also discuss the potential therapeutic role for targeting non-coding RNAs to treat these chronic lung diseases.

scholarly journals Hallmarks of the ageing lung

2015 ◽  
Vol 45 (3) ◽  
pp. 807-827 ◽  
Author(s):  
Silke Meiners ◽  
Oliver Eickelberg ◽  
Melanie Königshoff
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Specific Effects ◽  
Chronic Lung Diseases

Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, “dysregulation of the extracellular matrix”, which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases.

scholarly journals Comorbidity in idiopathic pulmonary fibrosis - what can biomarkers tell us?

2020 ◽  
Vol 14 ◽  
pp. 175346662091009 ◽  
Author(s):  
Tiago M. Alfaro ◽  
Carlos Robalo Cordeiro
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Clinical Manifestations ◽  
Premature Death ◽  
Sleep Apnoea ◽  
Significant Loss ◽  
Diagnostic Methods ◽  
Response To Treatment ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive parenchymal scarring, leading to dyspnoea, respiratory failure and premature death. Although IPF is confined to the lungs, the importance of IPF comorbidities such as pulmonary hypertension and ischaemic heart disease, lung cancer, emphysema/chronic obstructive pulmonary disease, gastroesophageal reflux, sleep apnoea and depression has been increasingly recognized. These comorbidities may be associated with increased mortality and significant loss of quality of life, so their identification and management are vital. The development of good-quality biomarkers could lead to numerous gains in the management of these patients. Biomarkers can be used for the identification of predisposed individuals, early diagnosis, assessment of prognosis, selection of best treatment and assessment of response to treatment. However, the role of biomarkers for IPF comorbidities is still quite limited, and mostly based on evidence coming from populations without IPF. The future development of new biomarker studies could be informed by those that have been studied independently for each of these conditions. For now, clinicians should be mostly attentive to clinical manifestations of IPF comorbidities, and use validated diagnostic methods for diagnosis. As research on biomarkers of most common diseases continues, it is expected that useful biomarkers are developed for these diseases and then validated for IPF populations. The reviews of this paper are available via the supplemental material section.

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