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Updated: May 28, 2025

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Klotho Regulates Club Cell Senescence and Differentiation in Chronic Obstructive Pulmonary Disease.

Min Li1,2,3, Bo Chen1,4,5, Sibo Sun6

  • 1Department of Geriatrics, Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Cell Proliferation
|February 11, 2025
PubMed
Summary
This summary is machine-generated.

Klotho deficiency worsens chronic obstructive pulmonary disease (COPD) by accelerating club cell senescence and lung inflammation. Targeting neddylation may reverse lung aging and club cell senescence in COPD.

Keywords:
chronic obstructive pulmonary diseaseclub cellklothoscRNA‐seqsenescence

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Area of Science:

  • Pulmonary Medicine
  • Aging Research
  • Cell Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) involves chronic inflammation and cellular senescence.
  • Club cells and their secretory proteins (CCSP) possess anti-inflammatory properties diminished in COPD.
  • Klotho (KL) levels are reduced in human COPD lung tissue, and KL deficiency in mice mimics COPD-like aging phenotypes.

Purpose of the Study:

  • To investigate the relationship between Klotho (KL), club cells, and COPD pathogenesis.
  • To explore how KL deficiency impacts club cell senescence and contributes to COPD-related inflammation.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of COPD lung tissue to analyze club cell heterogeneity and senescence.
  • Analysis of KL and CCSP expression in cigarette smoke (CS)-induced COPD mouse models.
  • Assessment of KL knockout effects on club cell differentiation and pulmonary inflammation.
  • In vitro studies using SA-β-gal staining to evaluate the role of hnRNPA2/B1 and neddylation in club cell senescence.

Main Results:

  • scRNA-seq revealed club cell heterogeneity and senescence in COPD lungs.
  • KL and CCSP expression decreased in CS-induced COPD mice, correlating with aging markers.
  • KL deficiency led to club cell disappearance, increased ciliated cells, aggravated club cell senescence, and worsened pulmonary inflammation.
  • hnRNPA2/B1 was identified as a key molecule in KL-regulated club cell senescence, with neddylation influencing hnRNPA2/B1 levels.

Conclusions:

  • Klotho (KL) regulates club cell senescence and differentiation.
  • KL deficiency exacerbates lung inflammation and club cell senescence in response to cigarette smoke, impacting ciliated cell function.
  • Targeting neddylation presents a potential therapeutic strategy for reversing lung aging and club cell senescence in COPD.