# Signaling pathways of marine-derived natural products on lung injury: from the in vivo perspective

**Authors:** Haitong Wang, Feng Qiu

PMC · DOI: 10.3389/fphar.2025.1716898 · Frontiers in Pharmacology · 2026-01-05

## TL;DR

This paper reviews how marine natural products protect the lungs by targeting key biological pathways in animal models.

## Contribution

It systematically summarizes in vivo mechanisms of marine-derived compounds in treating lung injury.

## Key findings

- Marine natural products regulate pathways like αvβ3-FAK/Src and TLR4/MyD88 to reduce lung injury.
- They protect alveolar structures by targeting inflammation and oxidative stress pathways.
- Current research lacks marine drugs specifically for lung injury, requiring further clinical translation.

## Abstract

Lung injury is characterized by impaired gas exchange, inflammatory responses, and abnormal tissue repair. In severe cases, it can progress to respiratory failure, posing a threat to public health. Marine natural products, due to their structural and biological activity diversity, show significant potential in the treatment of lung injury. This article systematically reviews the mechanism by which marine-derived natural products improve lung injury by regulating key signaling pathways in vivo. Studies have demonstrated that marine natural products target pathological processes such as inflammatory immunity and oxidative stress by regulating signaling pathways including αvβ3-FAK/Src, TLR4/MyD88, NF-κB, and Keap1-Nrf2/HO-1/STAT3, thereby exerting a significant protective effect on alveolar structures in lung injury models induced by stimuli such as radiation, OVA, LPS, and cigarette smoke. Currently, there is a lack of marine drugs specifically for lung injury, and in-depth research is needed to promote their translation into clinical medications.

## Linked entities

- **Genes:** PTK2 (protein tyrosine kinase 2) [NCBI Gene 5747], SRC (SRC proto-oncogene, non-receptor tyrosine kinase) [NCBI Gene 6714], MYD88 (MYD88 innate immune signal transduction adaptor) [NCBI Gene 4615], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], KEAP1 (kelch like ECH associated protein 1) [NCBI Gene 9817], GABPA (GA binding protein transcription factor subunit alpha) [NCBI Gene 2551], HMOX1 (heme oxygenase 1) [NCBI Gene 3162], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774]
- **Proteins:** TLR4 (toll like receptor 4)
- **Diseases:** respiratory failure (MONDO:0021113)

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, KEAP1 (kelch like ECH associated protein 1) [NCBI Gene 9817] {aka INrf2, KLHL19}, HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, SRC (SRC proto-oncogene, non-receptor tyrosine kinase) [NCBI Gene 6714] {aka ASV, SRC1, THC6, c-SRC, p60-Src}, PTK2 (protein tyrosine kinase 2) [NCBI Gene 5747] {aka FADK, FADK 1, FAK, FAK1, FRNK, PPP1R71}, MYD88 (MYD88 innate immune signal transduction adaptor) [NCBI Gene 4615] {aka IMD68, MYD88D, WM1}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}
- **Diseases:** inflammatory (MESH:D007249), Lung injury (MESH:D055370), respiratory failure (MESH:D012131)
- **Chemicals:** LPS (MESH:D008070)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12812905/full.md

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12812905/full.md

## References

89 references — full list in the complete paper: https://tomesphere.com/paper/PMC12812905/full.md

---
Source: https://tomesphere.com/paper/PMC12812905