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Exploratory Changes in Surfactant Protein D During Intermittent Hypoxia and Modulation by Galectin-3 Inhibition.

Saad Al-Anazi^1,2, Yasser A Alshawakir³, Syed Shahid Habib¹

¹Department of Physiology, College of Medicine, King Saud University, Riyadh 11461, Saudi Arabia.

Advances in Respiratory Medicine

|May 27, 2026

Summary

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Breathing

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This summary is machine-generated.

Surfactant Protein D (SP-D) levels change with obstructive sleep apnea (OSA) severity, suggesting alveolar stress. Galectin-3 (Gal-3) inhibition impacts surfactant homeostasis and cardiopulmonary injury differently based on OSA severity.

Area of Science:

Pulmonary Medicine
Sleep Medicine
Immunology

Background:

Surfactant Protein D (SP-D) is crucial for alveolar homeostasis.
Obstructive sleep apnea (OSA)-related intermittent hypoxia (IH) disrupts pulmonary surfactant.
SP-D's role in IH-induced alveolar stress requires further characterization.

Purpose of the Study:

To explore SP-D as a potential indicator of IH-induced alveolar stress.
To evaluate if Galectin-3 (Gal-3) inhibition modulates surfactant homeostasis.
To assess the impact of Gal-3 inhibition on IH-related cardiopulmonary injury.

Main Methods:

Forty male Sprague-Dawley rats were exposed to normoxia, moderate IH (MIH), or severe IH (SIH).
Groups received either a Gal-3 inhibitor (Modified Citrus Pectin) or a placebo.

Keywords:

alveolar integrity exploratory biomarker galectin-3 intermittent hypoxia modified citrus pectin obstructive sleep apnea surfactant protein D

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Outcomes included circulating SP-D, SP-B, inflammatory markers, and lung injury scores.

Main Results:

SP-D levels decreased with increasing IH severity, but this was not statistically significant due to variability.
Gal-3 inhibition increased SP-D levels, especially in severe IH, and restored SP-B levels suppressed by moderate IH.
Gal-3 inhibition attenuated cardiac injury in severe IH but exacerbated inflammation in moderate IH.

Conclusions:

SP-D alterations correlate with IH severity, indicating alveolar stress, but require larger cohorts for biomarker validation.
Gal-3 inhibition shows context-dependent effects on surfactant homeostasis and cardiopulmonary injury.
Further research is needed to validate SP-D for OSA severity stratification and Gal-3 inhibition as a targeted anti-inflammatory therapy.