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The genetic basis of emphysema is complex, and risk factors for emphysema development remain incompletely defined. In the current study, follistatin-like 1 (FSTL-1) hypomorphic mice developed spontaneous emphysema, suggesting that FSTL-1 function in the lung is critical for lung homeostasis. FSTL-1 hypomorphic mice revealed altered immunoregulatory gene expression, including reduced Nr4a1. Exogenous FSTL-1 treatment of macrophages suppressed NF-kB p65 phosphorylation in an Nr4a1-dependent manner. Human SNP analysis of the FSTL1 locus identified a correlation with COPD status and lung function.

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This page is a summary of: FSTL-1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema, American Review of Respiratory Disease, April 2020, American Thoracic Society,
DOI: 10.1164/rccm.201905-0973oc.
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