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Background <p>Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury and is frequently associated with remote organ dysfunction, particularly acute lung injury (ALI). However, the molecular mechanisms underlying early kidney–lung crosstalk following renal IRI remain incompletely understood. Wnt/β-catenin signaling, which regulates inflammation, apoptosis, and tissue remodeling in pulmonary diseases, has not been adequately investigated in renal IRI-associated lung injury.</p> Methods <p>This study investigated early molecular events involved in kidney–lung crosstalk during the acute reperfusion phase following renal IRI. Male BALB/c mice were randomly assigned to control or renal IRI groups (<i>n</i> = 7 per group). Renal IRI was induced by 30&#xa0;min of bilateral renal artery occlusion followed by 6&#xa0;h of reperfusion. Lung injury was evaluated histologically and by determination of the lung wet/dry weight ratio. Pulmonary levels of Wnt-4, β-catenin, neutrophil gelatinase-associated lipocalin (NGAL), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), p53, Bax, and Bcl-2 were measured using enzyme-linked immunosorbent assay. Apoptosis was assessed by TUNEL staining.</p> Results <p>Renal IRI resulted in significant pulmonary histopathological injury and edema accompanied by increased pulmonary expression of Wnt-4 and β-catenin, elevated NGAL and pro-inflammatory cytokine levels, and enhanced apoptotic signaling. Increased apoptosis was evidenced by p53 and Bax upregulation, an elevated Bax/Bcl-2 ratio, and increased numbers of TUNEL-positive cells in lung tissue.</p> Conclusion <p>During the early reperfusion phase, renal IRI is associated with pulmonary inflammation and apoptosis, accompanied by increased Wnt-4 and β-catenin expression in lung tissue. These findings provide further insight into acute-phase mechanisms of kidney–lung crosstalk and suggest that Wnt/β-catenin signaling may contribute to remote lung injury following renal ischemia–reperfusion.</p>

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Early Activation of the Wnt/β-Catenin Signaling Pathway is Associated with Acute Lung Injury Following Renal Ischemia–Reperfusion in Mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月14日

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  • Meltem Kumaş,
  • Kadri Kulualp,
  • Zeynep Semen,
  • Gökçen Güvenç Bayram,
  • Aslı Çelik,
  • Melek Yeşim AK,
  • Osman Yilmaz

摘要

Background

Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury and is frequently associated with remote organ dysfunction, particularly acute lung injury (ALI). However, the molecular mechanisms underlying early kidney–lung crosstalk following renal IRI remain incompletely understood. Wnt/β-catenin signaling, which regulates inflammation, apoptosis, and tissue remodeling in pulmonary diseases, has not been adequately investigated in renal IRI-associated lung injury.

Methods

This study investigated early molecular events involved in kidney–lung crosstalk during the acute reperfusion phase following renal IRI. Male BALB/c mice were randomly assigned to control or renal IRI groups (n = 7 per group). Renal IRI was induced by 30 min of bilateral renal artery occlusion followed by 6 h of reperfusion. Lung injury was evaluated histologically and by determination of the lung wet/dry weight ratio. Pulmonary levels of Wnt-4, β-catenin, neutrophil gelatinase-associated lipocalin (NGAL), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), p53, Bax, and Bcl-2 were measured using enzyme-linked immunosorbent assay. Apoptosis was assessed by TUNEL staining.

Results

Renal IRI resulted in significant pulmonary histopathological injury and edema accompanied by increased pulmonary expression of Wnt-4 and β-catenin, elevated NGAL and pro-inflammatory cytokine levels, and enhanced apoptotic signaling. Increased apoptosis was evidenced by p53 and Bax upregulation, an elevated Bax/Bcl-2 ratio, and increased numbers of TUNEL-positive cells in lung tissue.

Conclusion

During the early reperfusion phase, renal IRI is associated with pulmonary inflammation and apoptosis, accompanied by increased Wnt-4 and β-catenin expression in lung tissue. These findings provide further insight into acute-phase mechanisms of kidney–lung crosstalk and suggest that Wnt/β-catenin signaling may contribute to remote lung injury following renal ischemia–reperfusion.