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Refined Murine Model of Idiopathic Pulmonary Fibrosis

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CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.

Huachun Cui¹, Na Xie¹, Sami Banerjee¹

¹Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.

American Journal of Respiratory and Critical Care Medicine

|June 10, 2022

Summary

Targeting CD38 in alveolar cells may treat lung fibrosis. This enzyme drives cellular aging and worsens fibrosis by depleting NAD. Inhibiting CD38 shows promise for new therapies.

Keywords:

CD38 alveolar epithelial cell nicotinamide adenine dinucleotide pulmonary fibrosis senescence

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Area of Science:

Pulmonary Medicine
Cellular Biology
Aging Research

Background:

Idiopathic pulmonary fibrosis (IPF) involves alveolar epithelial cell (AEC) injury and aging.
The specific factors driving AEC aging in fibrosis remain unclear.
Developing strategies to reduce AEC aging and disease progression is crucial.

Purpose of the Study:

To investigate the role of AEC CD38 (cluster of differentiation 38) in cellular aging and lung fibrosis.
To determine if CD38 is a viable therapeutic target for IPF.

Main Methods:

Single-cell RNA sequencing
Real-time PCR
Flow cytometry
Western blotting
Analysis of human IPF lung tissue and mouse models of lung fibrosis.

Main Results:

CD38 expression is elevated in IPF lungs and inversely correlates with lung function.
Increased CD38 in AECs promotes cellular aging and lung fibrosis in mice, particularly in older animals.
CD38 downregulation of nicotinamide adenine dinucleotide (NAD) impairs cellular functions.
Genetic or pharmacological inhibition of CD38 ameliorates lung fibrosis and improves NAD-dependent activities.

Conclusions:

Alveolar CD38 plays a critical role in AEC aging and the pathogenesis of lung fibrosis.
Targeting CD38 represents a novel therapeutic strategy for treating IPF.
Modulating CD38 could reverse aging-related cellular dysfunction and mitigate fibrotic processes.