FAM13A variants influence tissue destruction in COPD and fibrotic remodeling in pulmonary fibrosis

Photo by Logan Voss / Unsplash

Frontiers in Medicine Published June 2, 2026 Medically reviewed June 2, 2026 DOI ↗ By Dr. Julia Lee, PhD · Oncology, Genomics & Drug Development

Key Takeaway

Note FAM13A associations with tissue destruction in COPD and mitigated fibrosis in pulmonary fibrosis.

This narrative review explores the biological role of the FAM13A gene across several respiratory conditions. The scope includes chronic obstructive pulmonary disease, pulmonary fibrosis, asthma, and lung cancer, though specific population details were not reported.

Key synthesized findings indicate that FAM13A is associated with tissue destruction in chronic obstructive pulmonary disease. In the context of pulmonary fibrosis, the gene is linked to mitigated fibrotic remodeling. The review does not provide absolute numbers, p-values, or confidence intervals for these associations.

The authors highlight several limitations that affect interpretation. These include the complexity introduced by multiple splice variants, interspecies expression differences, and environmental dependence. Because this is a narrative review, causal language is avoided and certainty is tempered by the lack of primary trial data.

The practice relevance centers on implications for future research and precision medicine. No adverse events or specific medication data were included in this source.

Study Details

Study typeSystematic review

EvidenceLevel 1

PublishedMay 2026

View Original Abstract ↓

FAM13A, a lung-enriched gene encoding a protein with a characteristic RhoGAP domain, is increasingly recognized for its pleiotropic roles across multiple lung diseases, including chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (PF), asthma, and lung cancer. Through modulation of Rho and Wnt/β-catenin signaling, FAM13A regulates key cellular processes such as epithelial barrier maintenance, immune homeostasis, and cell-cycle regulation. Notably, FAM13A exhibits context-dependent duality, associated with tissue destruction in COPD while linked to mitigated fibrotic remodeling in PF. In addition, the complexity introduced by multiple splice variants, interspecies expression differences, and environmental dependence poses significant challenges for further mechanistic studies of FAM13A. By emphasizing the opposing roles of FAM13A in COPD versus PF, the non-linear relationships linking single-nucleotide polymorphisms (SNPs), gene expression, signaling pathways, and disease phenotypes, as well as the combined influence of isoform diversity, species differences, and environmental exposures on functional outcomes, this review integrates current genetic, molecular, and functional evidence to provide a mechanistic framework for understanding FAM13A’s roles in pulmonary diseases and refines current paradigms with implications for future research and precision medicine.