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Peer-reviewedCC BY 4.0Frontiers in Medicine

Metabolic reprogramming in pulmonary fibrosis: mechanisms and therapeutic perspectives

  • Yaoqiao Wu1
  • Xiaojing Su1
  • Jingrun Zhou2
  • Shaomao Zheng2
  • Qiong Feng2
  • Jingying Zhuang1
  • Ziyi Yu1
  • Hangqi Qiu1
  • Yang Xia1
  • Juanjuan Wu1
  • Chengji Jin2
  • Jing Wang1,2
  1. 1Hainan Medical University, Haikou, Hainan, China
  2. 2Department of Respiratory Medicine, Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China
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Abstract

Pulmonary fibrosis is a fatal disease characterized by progressive destruction of the lung parenchyma and excessive deposition of extracellular matrix, and is marked by a complex pathogenesis and limited treatment options. In recent years, metabolic reprogramming has emerged as a central mechanism by which cells adapt to stress and contribute to disease progression, attracting considerable interest within pulmonary fibrosis research. This review summarizes the metabolic reprogramming of key effector cells involved in pulmonary fibrosis, including lung fibroblasts, alveolar epithelial cells, macrophages, and endothelial cells, focusing on glucose, lipid, and amino acid metabolic pathways. It elucidates how these metabolic alterations drive fibrotic progression by influencing cell activation, proliferation, apoptosis, and intercellular communication. Building on these mechanistic insights, the review further summarizes potential therapeutic strategies targeting various metabolic pathways, aiming to establish a theoretical foundation and strategic directions for the development of novel precision therapies for pulmonary fibrosis. Furthermore, we highlight the metabolic communication among different pulmonary cell populations and discuss emerging challenges for precision metabolic therapies.

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Cite

BibTeXRIS
BibTeX
@article{wu2026metabolic,
  title = {{Metabolic reprogramming in pulmonary fibrosis: mechanisms and therapeutic perspectives}},
  author = {Yaoqiao Wu and Xiaojing Su and Jingrun Zhou and Shaomao Zheng and Qiong Feng and Jingying Zhuang and Ziyi Yu and Hangqi Qiu and Yang Xia and Juanjuan Wu and Chengji Jin and Jing Wang},
  journal = {Frontiers in Medicine},
  year = {2026},
  month = oct,
  doi = {10.3389/fmed.2026.1982119},
  url = {https://doi.org/10.3389/fmed.2026.1982119},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Metabolic reprogramming in pulmonary fibrosis: mechanisms and therapeutic perspectives
AU  - Yaoqiao Wu
AU  - Xiaojing Su
AU  - Jingrun Zhou
AU  - Shaomao Zheng
AU  - Qiong Feng
AU  - Jingying Zhuang
AU  - Ziyi Yu
AU  - Hangqi Qiu
AU  - Yang Xia
AU  - Juanjuan Wu
AU  - Chengji Jin
AU  - Jing Wang
PY  - 2026
DA  - 2026/10/22
JO  - Frontiers in Medicine
DO  - 10.3389/fmed.2026.1982119
UR  - https://doi.org/10.3389/fmed.2026.1982119
AB  - Pulmonary fibrosis is a fatal disease characterized by progressive destruction of the lung parenchyma and excessive deposition of extracellular matrix, and is marked by a complex pathogenesis and limited treatment options. In recent years, metabolic reprogramming has emerged as a central mechanism by which cells adapt to stress and contribute to disease progression, attracting considerable interest within pulmonary fibrosis research. This review summarizes the metabolic reprogramming of key effector cells involved in pulmonary fibrosis, including lung fibroblasts, alveolar epithelial cells, macrophages, and endothelial cells, focusing on glucose, lipid, and amino acid metabolic pathways. It elucidates how these metabolic alterations drive fibrotic progression by influencing cell activation, proliferation, apoptosis, and intercellular communication. Building on these mechanistic insights, the review further summarizes potential therapeutic strategies targeting various metabolic pathways, aiming to establish a theoretical foundation and strategic directions for the development of novel precision therapies for pulmonary fibrosis. Furthermore, we highlight the metabolic communication among different pulmonary cell populations and discuss emerging challenges for precision metabolic therapies.
SN  - 2296-858X
ER  -