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Matricellular Regulation of Alveolar Epithelial Cell Plasticity in Neonatal Lung Injury: Insights from CCN5 and

Najla Fiaturi1,2, Heber C Nielsen3, John Castellot1,2

  • 1Department of Medical Education, Tufts University School of Medicine, Boston MA, USA.

Medical Research Archives
|April 6, 2026
PubMed

Insights

Neonatal lung injury, a cause of bronchopulmonary dysplasia (BPD), involves arrested lung development. CCN5 (WISP2) protein shows potential in promoting lung repair and resilience in premature infants.

Area of Science:

  • Neonatal medicine
  • Cellular biology
  • Regenerative medicine

Background:

  • Neonatal lung injury is a significant cause of morbidity in preterm infants, leading to bronchopulmonary dysplasia (BPD).
  • Understanding lung repair mechanisms is crucial for improving outcomes in premature infants.
  • Matricellular proteins, including the CCN family, play key roles in modulating epithelial responses to injury.

Purpose of the Study:

  • To examine the specific role of CCN5 (WISP2) in alveolar epithelial cell (AEC) plasticity during neonatal lung injury.
  • To elucidate how CCN5 influences epithelial survival, epithelial-mesenchymal transition (EMT), mitochondrial function, and signaling in hyperoxic injury.
  • To position CCN5 within broader matricellular signaling networks and contrast it with other CCN members in lung disease.

Main Methods:

  • Review of existing literature on CCN family proteins and neonatal lung injury.
  • Integration of the authors' research findings on CCN5 function.
  • Analysis of CCN5's influence on AEC plasticity, EMT, mitochondrial homeostasis, and intercellular signaling in hyperoxic injury models.

Main Results:

  • CCN5 (WISP2) modulates AEC plasticity, influencing epithelial survival and epithelial-mesenchymal transition (EMT).
  • CCN5 impacts mitochondrial homeostasis and intercellular signaling pathways in response to hyperoxic injury.
  • CCN5's role in neonatal lung injury differs from other CCN members implicated in fibrotic lung diseases.

Conclusions:

  • CCN5 (WISP2) is a key mediator of epithelial resilience and tissue homeostasis in neonatal lung injury.
  • CCN5 represents a potential therapeutic target for mitigating bronchopulmonary dysplasia (BPD) and enhancing lung regeneration in premature infants.

Keywords:
CCN5alveolar epithelial cellsbronchopulmonary dysplasiaepithelial plasticityextracellular matrixmatricellular signalingneonatal lung injuryregenerative biology

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