ArticleClinical science (London, England : 1979)2015
Klotho expression is reduced in COPD airway epithelial cells: effects on inflammation and oxidant injury.
Article in Clinical science (London, England : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05173194 (Effects of a Remotely Supervised Exercise Program on Inflammatory Markers, Muscle Strength and Lung Function in Adult Patients With Cystic Fibrosis), which is not on this map. Cited by 53 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Effects of a Remotely Supervised Exercise Program on Inflammatory Markers, Muscle Strength and Lung Function in Adult Patients With Cystic Fibrosis
Who cites it
53 citing papers in PubMed, 100 citations in OpenAlex.
- Comparative Diagnostic Performance of Serum α-Klotho and FGF-23 in Predicting Obstructive Sleep Apnea Severity: A Novel Biomarker Approach.Journal of clinical medicine · 2026Article
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Reduced serum Klotho in chronic schizophrenia: diagnostic value and association with cognitive impairment.Frontiers in psychiatry · 2026Article
- Klotho Regulates Club Cell Senescence and Differentiation in Chronic Obstructive Pulmonary Disease.Cell proliferation · 2025Article
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.Respiratory research · 2025Article
- The prognostic value of serum α-klotho in age-related diseases among the US population: A prospective population-based cohort study.Preventive medicine reports · 2024Article
- Review
- Analysis of the correlation between serum Klotho and FeNO: a cross-sectional study from NHANES (2007-2012).BMC pulmonary medicine · 2024Article
- Association between α-klotho levels and adults with COPD in the United States.Frontiers in medicine · 2024Article
- The aging lung: microenvironment, mechanisms, and diseases.Frontiers in immunology · 2024Review
- Oxidative stress in the brain-lung crosstalk: cellular and molecular perspectives.Frontiers in aging neuroscience · 2024Review
- Association Between Serum Klotho and Chronic Obstructive Pulmonary Disease in US Middle-Aged and Older Individuals: A Cross-Sectional Study from NHANES 2013-2016.International journal of chronic obstructive pulmonary disease · 2024Article
- Role of mitochondrial fusion proteins MFN2 and OPA1 on lung cellular senescence in chronic obstructive pulmonary disease.Respiratory research · 2023Article
- Serum α-Klotho level, lung function, airflow obstruction and inflammatory markers in US adults.ERJ open research · 2023Article
- TIMP-1 and its potential diagnostic and prognostic value in pulmonary diseases.Chinese medical journal pulmonary and critical care medicine · 2023Article
- The Role of Oxidative Stress and Antioxidants in Cardiovascular Comorbidities in COPD.Antioxidants (Basel, Switzerland) · 2023Review
- Bufei Yishen Formula Inhibits the Cell Senescence in COPD by Up-Regulating the ZNF263 and Klotho Expression.International journal of chronic obstructive pulmonary disease · 2023Article
- The fibroblast growth factor-Klotho axis at molecular level.Open life sciences · 2023Review
- Comparative transcriptomics in human COPD reveals dysregulated genes uniquely expressed in ferrets.Respiratory research · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
COPD (chronic obstructive pulmonary disease) is associated with sustained inflammation, excessive injury, and accelerated lung aging. Human Klotho (KL) is an anti-aging protein that protects cells against inflammation and damage. In the present study, we quantified KL expression in the lungs of COPD patients and in an ozone-induced mouse model of COPD, and investigated the mechanisms that control KL expression and function in the airways. KL distribution and levels in human and mouse airways were measured by immunohistochemistry and Western blotting. The effect of CSE (cigarette smoke extract) on KL expression was detected in human bronchial epithelial cells. Moreover, the effect of KL on CSE-mediated inflammation and hydrogen peroxide-induced cellular injury/apoptosis was determined using siRNAs. KL expression was decreased in the lungs of smokers and further reduced in patients with COPD. Similarly, 6 weeks of exposure to ozone decreased KL levels in airway epithelial cells. CSE and TNFα (tumour necrosis factor α) decreased KL expression and release from airway epithelial cells, which was associated with enhanced pro-inflammatory cytokine expression. Moreover, KL depletion increased cell sensitivity to cigarette smoke-induced inflammation and oxidative stress-induced cell damage. These effects involved the NF-κB (nuclear factor κB), MAPK (mitogen-activated protein kinase) and Nrf2 (nuclear factor erythroid 2-related factor 2) pathways. Reduced KL expression in COPD airway epithelial cells was associated with increased oxidative stress, inflammation and apoptosis. These data provide new insights into the mechanisms associated with the accelerated lung aging in COPD development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.