In the last decade the concept of aging-associated mechanisms, such as cellular senescence, that contribute to the development of respiratory diseases has emerged. Telomeres, being major drivers of senescence, are repetitive DNA sequences at the ends of chromosomes critical for the maintenance of genomic integrity. Telomere shortening has been implicated in a variety of lung diseases as idiopathic pulmonary fibrosis, COPD, emphysema, chronic asthma and lung cancer. It is also important to highlight mutations in genes related to telomere length that were found in cases of familial Idiopathic Pulmonary Fibrosis. Shorter telomeres were associated with severity and persistence of the disease in the case of asthma. Furthermore, telomere dysfunction and activation of senescence markers in the airways of patients with bronchiectasis has been documented. Likewise, telomere dysfunction and senescence are thought to contribute to impaired cellular regeneration and the proinflammatory phenotype in COPD, an accelerated aging disease as recently proposed.
Although telomere shortening has been implicated in a variety of lung diseases, there are still many questions to be answered. What do we know about telomere attrition in relation to respiratory diseases development and progression? Could telomere attrition serve as a biomarker of disease? Could telomere shortening represent a future therapeutic target? Undoubtedly, there is a need to expand research assessing telomere dysfunction and the physiology of the aging lung in relation to disease development and progression.
In this Research Topic, recent advances in the basic and clinical research on telomere dysfunction in relation to certain lung diseases will be presented. Topics of interest include, but are not limited to:
• Novel mechanisms of telomere dysfunction in lung diseases
• Telomere shortening in relation to disease development and progression
• Telomere dysfunction and risk of disease outcomes
• Telomere length and therapeutics
Here, original research, systematic reviews and mini-reviews will be accepted.
In the last decade the concept of aging-associated mechanisms, such as cellular senescence, that contribute to the development of respiratory diseases has emerged. Telomeres, being major drivers of senescence, are repetitive DNA sequences at the ends of chromosomes critical for the maintenance of genomic integrity. Telomere shortening has been implicated in a variety of lung diseases as idiopathic pulmonary fibrosis, COPD, emphysema, chronic asthma and lung cancer. It is also important to highlight mutations in genes related to telomere length that were found in cases of familial Idiopathic Pulmonary Fibrosis. Shorter telomeres were associated with severity and persistence of the disease in the case of asthma. Furthermore, telomere dysfunction and activation of senescence markers in the airways of patients with bronchiectasis has been documented. Likewise, telomere dysfunction and senescence are thought to contribute to impaired cellular regeneration and the proinflammatory phenotype in COPD, an accelerated aging disease as recently proposed.
Although telomere shortening has been implicated in a variety of lung diseases, there are still many questions to be answered. What do we know about telomere attrition in relation to respiratory diseases development and progression? Could telomere attrition serve as a biomarker of disease? Could telomere shortening represent a future therapeutic target? Undoubtedly, there is a need to expand research assessing telomere dysfunction and the physiology of the aging lung in relation to disease development and progression.
In this Research Topic, recent advances in the basic and clinical research on telomere dysfunction in relation to certain lung diseases will be presented. Topics of interest include, but are not limited to:
• Novel mechanisms of telomere dysfunction in lung diseases
• Telomere shortening in relation to disease development and progression
• Telomere dysfunction and risk of disease outcomes
• Telomere length and therapeutics
Here, original research, systematic reviews and mini-reviews will be accepted.
