Short telomeres: a repeat offender in IPF

Stanley, Susan E.; Armanios, Mary

doi:10.1016/s2213-2600(14)70140-7

Cited by 9 publications

(5 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Individuals with progeria syndromes are also at higher risk of fibrotic disorders [25] , [26] . Recent studies indicate that shortened telomere length is a risk factor for IPF [27] , and IPF is the most common disorder in telomere dysfunction syndromes [28] . The risk of liver fibrosis with chronic viral infections and alcohol exposure also increase with aging [29] .…”

Section: Fibrosis Is a Disease Of Agingmentioning

confidence: 99%

Redox mechanisms in age-related lung fibrosis

Kurundkar

Thannickal

2016

Redox Biology

View full text Add to dashboard Cite

Redox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are deficient with aging and cellular senescence, leading to redox imbalance and oxidative stress. However, the precise mechanisms by which redox signaling and oxidative stress contribute to the pathogenesis of lung fibrosis are not well understood. Tissue repair is a highly regulated process that involves the interactions of several cell types, including epithelial cells, fibroblasts and inflammatory cells. Fibrosis may develop when these interactions are dysregulated with the acquisition of pro-fibrotic cellular phenotypes. In this review, we explore the roles of redox mechanisms that promote and perpetuate fibrosis in the context of cellular senescence and aging.

show abstract

Section: Fibrosis Is a Disease Of Agingmentioning

confidence: 99%

Redox mechanisms in age-related lung fibrosis

Kurundkar

Thannickal

2016

Redox Biology

View full text Add to dashboard Cite

show abstract

“…Patient diagnosed of progeria syndromes are also at a higher possibility of fibrotic disorder 48 . Telomere dysfunction syndromes and the short telomere length is a dangerous factor in an individual with IPF 49 .…”

Section: Introductionmentioning

confidence: 99%

Alveolar type 2 progenitor cells for lung injury repair

Olajuyin

Zhang

2019

Cell Death Discovery

134

122

View full text Add to dashboard Cite

Alveolar type 2 progenitor cells (AT2) seem closest to clinical translation, specifying the evidence that AT2 may satisfactorily control the immune response to decrease lung injury by stabilizing host immune-competence and a classic and crucial resource for lung regeneration and repair. AT2 establish potential in benefiting injured lungs. However, significant discrepancies linger in our understanding vis-à-vis the mechanisms for AT2 as a regime for stem cell therapy as well as essential guiding information for clinical trials, including effectiveness in appropriate pre-clinical models, safety, mostly specifications for divergent lung injury patients. These important gaps shall be systematically investigated prior to the vast therapeutic perspective of AT2 cells for pulmonary diseases can be considered. This review focused on AT2 cells homeostasis, pathophysiological changes in the pathogenesis of lung injury, physiological function of AT2 cells, apoptosis of AT2 cells in lung diseases, the role of AT2 cells in repairing processes after lung injury, mechanism of AT2 cells activation promote repairing processes after lung injury, and potential therapy of lung disease by utilizing the AT2 progenitor cells. The advancement remains to causally connect the molecular and cellular alteration of AT2 cells to lung injury and repair. Conclusively, it is identified that AT2 cells can convert into AT1 cells; but, the comprehensive cellular mechanisms involved in this transition are unrevealed. Further investigation is mandatory to determine new strategies to prevent lung injury.

show abstract

“…Telomere homeostasis and maintenance is one of the best-described parameters of aging (35). Telomere dysfunction underlies many diseases and may lower the threshold for a "second hit" to manifest disease attributes (36,37).…”

mentioning

confidence: 99%

Aging and Lung Disease. Clinical Impact and Cellular and Molecular Pathways

et al. 2015

View full text Add to dashboard Cite

With the expected rapid growth of the aging population worldwide, there is a clear need to understand the complex process of aging to develop interventions that might extend the health span in this group of patients. Aging is associated with increased susceptibility to a variety of chronic diseases, and lung pathologies are no exception. The prevalence of lung diseases such as idiopathic pulmonary fibrosis and chronic obstructive pulmonary disease has been found to increase considerably with age. In October 2014, the Division of Pulmonary, Allergy, and Critical Care of the University of Pittsburgh cohosted the Pittsburgh-Munich Lung Conference focused in aging and lung disease with the Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Ludwig-Maximilians University and Helmholtz Zentrum Munich Germany. The purpose of the conference was to disseminate novel concepts in aging mechanisms that have an impact in lung physiology and pathogenesis of pulmonary diseases that commonly occur in older populations. The conference included 28 presentations on diverse topics, which are summarized in this report. The participants identified priorities for future basic and translational investigations that will assist in the identification of molecular insights involved in the pathogenesis of age-related pulmonary diseases and the design of therapeutic interventions for these lung conditions.

show abstract

Short telomeres: a repeat offender in IPF

Cited by 9 publications

References 11 publications

Redox mechanisms in age-related lung fibrosis

Redox mechanisms in age-related lung fibrosis

Alveolar type 2 progenitor cells for lung injury repair

Aging and Lung Disease. Clinical Impact and Cellular and Molecular Pathways

Contact Info

Product

Resources

About