Targeting SRSF7 offers potential therapy for pulmonary fibrosis

This new article publication from Acta Pharmaceutica Sinica B, discusses how SRSF7 promotes pulmonary fibrosis through regulating PKM alternative splicing in lung fibroblasts.

Idiopathic pulmonary fibrosis (IPF), a chronic interstitial lung disease, is characterized by aberrant wound healing, excessive scarring and the formation of myofibroblastic foci. Although the role of alternative splicing (AS) in the pathogenesis of organ fibrosis has garnered increasing attention, its specific contribution to pulmonary fibrosis remains incompletely understood.

In this study, an up-regulation of serine/arginine-rich splicing factor 7 (SRSF7) was identified in lung fibroblasts derived from IPF patients and a bleomycin (BLM)-induced mouse model, and further characterized its functional role in both human fetal lung fibroblasts and mice.

It was demonstrated that enhanced expression of Srsf7 in mice spontaneously induced alveolar collagen accumulation. Mechanistically, alternative splicing events were investigated and revealed that SRSF7 modulates the alternative splicing of pyruvate kinase (PKM), leading to metabolic dysregulation and fibroblast activation.

In vivo studies showed that fibroblast-specific knockout of Srsf7 in conditional knockout mice conferred resistance to bleomycin-induced pulmonary fibrosis. Importantly, through drug screening, lomitapide was identified as a novel modulator of SRSF7, which effectively mitigated experimental pulmonary fibrosis.

Collectively, these findings elucidate a molecular pathway by which SRSF7 drives fibroblast metabolic dysregulation and propose a potential therapeutic strategy for pulmonary fibrosis.

Source:
Journal reference:

Jin, T., et al. (2025). SRSF7 promotes pulmonary fibrosis through regulating PKM alternative splicing in lung fibroblasts. Acta Pharmaceutica Sinica B. doi.org/10.1016/j.apsb.2025.04.017.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
AI-designed drug shows early promise for lung fibrosis patients in clinical trial