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Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

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The interplay between lung galectins and pro-fibrotic markers in post-COVID-19 fibrogenesis: A pilot study.

Daniela Oatis1, Cornel Balta2, Hildegard Herman2

  • 1Multidisciplinary Doctoral School, "Vasile Goldis" Western University of Arad, 310144 Arad, Romania; Department of Infectious Disease, Faculty of Medicine, "Vasile Goldis" Western University of Arad, 310144 Arad, Romania.

Life Sciences
|December 21, 2024
PubMed
Summary
This summary is machine-generated.

COVID-19 can cause lung fibrosis. This study found that galectins-1 and -3 increase over time post-infection and correlate with fibrotic markers, suggesting they are potential therapeutic targets for treating COVID-19 lung damage.

Keywords:
CTGFCovid-19Gal-1Gal-3Lung fibrosisTGFβαSMA

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Area of Science:

  • Pulmonology and Respiratory Medicine
  • Immunology and Inflammation
  • Molecular Biology and Virology

Background:

  • COVID-19, caused by SARS-CoV-2, is associated with severe lung complications, including interstitial pulmonary fibrosis.
  • Understanding the molecular mechanisms driving post-COVID-19 lung fibrosis is crucial for developing effective treatments.
  • Galectins are implicated in fibrotic processes, but their specific role in COVID-19-associated fibrosis requires further investigation.

Purpose of the Study:

  • To investigate the progression of fibrosis markers in patients following COVID-19 infection.
  • To examine the role of galectins-1 and -3 in the development of COVID-19-related lung fibrosis.
  • To identify potential molecular targets for therapeutic intervention in post-COVID-19 lung disease.

Main Methods:

  • Serial bronchoalveolar lavage (BAL) samples were collected from 16 COVID-19 patients at 1, 3, and 6 months post-infection.
  • BAL samples from 10 healthy controls were used for comparison.
  • RT-PCR, ELISA, and immunofluorescence were employed to quantify fibrosis markers (αSMA, TGFβ, CTGF) and galectins-1 and -3.

Main Results:

  • Increased α-smooth muscle actin (αSMA)-positive macrophages were observed at 6 months post-infection.
  • Elevated levels of αSMA, TGFβ, and CTGF mRNA and proteins were detected at 6 months compared to controls.
  • Galectin-1 and galectin-3 concentrations increased over time and significantly correlated with pro-fibrotic markers.

Conclusions:

  • Galectins-1 and -3 play a significant role in the progression of lung fibrosis following COVID-19.
  • These galectins are potential biomarkers for monitoring fibrotic progression.
  • Targeting galectins may offer a novel therapeutic strategy for mitigating COVID-19-induced pulmonary fibrosis.