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Peer-reviewedCC BY-NC 4.0International Journal of Nanomedicine

Extracellular Vesicles and Choline Metabolism in Neonatal Bronchopulmonary Dysplasia: A Systems-Pharmacology Framework for Regenerative Therapy

  • Radhika Joshi1,2
  • Aarti Deshwal1
  • Hitisha Sharma1
  • Manshi Kesharwani1
  • Swati Paliwal1
  • Devesh U Kapoor3
  • Swapnil Sharma1
  1. 1Department of Pharmacy, Banasthali Vidyapith, Banasthali, Rajasthan, India
  2. 2Department of Bioscience & Biotechnology, Banasthali Vidyapith, Banasthali, Rajasthan, India
  3. 3Department of Pharmacy, Dr. Dayaram Patel Pharmacy College, Surat, Gujrat, India
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Abstract

Bronchopulmonary dysplasia (BPD) affects not only the lungs but also the lung–brain axis, leading to neuroinflammation and white matter dysmaturation. Current therapies for BPD treat the lung manifestations but do not address the multi-organistic signaling network essential for neonatal development. Here, we describe a regenerative medicine-based approach to treat BPD by employing the extracellular vesicle (EV) and choline pathways to restore developmental homeostasis. Mesenchymal cell-derived EVs transport bioactive lipids, proteins, and microRNAs to target cells to resolve inflammation and stabilize the endothelial barrier. At the same time, choline and its derivatives regulate phosphatidylcholine and S-adenosylmethionine synthesis to preserve cellular membrane integrity and epigenetic marks. The systems-pharmacology hypothesis that EV-mediated signaling and choline-dependent phospholipid and one-carbon metabolism may have complementary effects on inflammatory, vascular, and neurodevelopmental pathways is supported by available mechanistic evidence. Thus, the combined effect of the EV and choline pathways represents a highly translational and network-based therapy to treat BPD and protect the lung–brain axis.

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Cite

BibTeXRIS
BibTeX
@article{joshi2026extracellular,
  title = {{Extracellular Vesicles and Choline Metabolism in Neonatal Bronchopulmonary Dysplasia: A Systems-Pharmacology Framework for Regenerative Therapy}},
  author = {Radhika Joshi and Aarti Deshwal and Hitisha Sharma and Manshi Kesharwani and Swati Paliwal and Devesh U Kapoor and Swapnil Sharma},
  journal = {International Journal of Nanomedicine},
  year = {2026},
  month = oct,
  doi = {10.2147/ijn.s639450},
  url = {https://doi.org/10.2147/ijn.s639450},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Extracellular Vesicles and Choline Metabolism in Neonatal Bronchopulmonary Dysplasia: A Systems-Pharmacology Framework for Regenerative Therapy
AU  - Radhika Joshi
AU  - Aarti Deshwal
AU  - Hitisha Sharma
AU  - Manshi Kesharwani
AU  - Swati Paliwal
AU  - Devesh U Kapoor
AU  - Swapnil Sharma
PY  - 2026
DA  - 2026/10/26
JO  - International Journal of Nanomedicine
DO  - 10.2147/ijn.s639450
UR  - https://doi.org/10.2147/ijn.s639450
AB  - Bronchopulmonary dysplasia (BPD) affects not only the lungs but also the lung–brain axis, leading to neuroinflammation and white matter dysmaturation. Current therapies for BPD treat the lung manifestations but do not address the multi-organistic signaling network essential for neonatal development. Here, we describe a regenerative medicine-based approach to treat BPD by employing the extracellular vesicle (EV) and choline pathways to restore developmental homeostasis. Mesenchymal cell-derived EVs transport bioactive lipids, proteins, and microRNAs to target cells to resolve inflammation and stabilize the endothelial barrier. At the same time, choline and its derivatives regulate phosphatidylcholine and S-adenosylmethionine synthesis to preserve cellular membrane integrity and epigenetic marks. The systems-pharmacology hypothesis that EV-mediated signaling and choline-dependent phospholipid and one-carbon metabolism may have complementary effects on inflammatory, vascular, and neurodevelopmental pathways is supported by available mechanistic evidence. Thus, the combined effect of the EV and choline pathways represents a highly translational and network-based therapy to treat BPD and protect the lung–brain axis.
SN  - 1176-9114
SN  - 1178-2013
ER  -