Percolation Forces in Lung Inflammation: Determining the Path to Emphysema or Fibrosis

The dichotomous outcomes of chronic lung inflammation, represented by either pulmonary emphysema or interstitial fibrosis, involve poorly understood overlapping mechanisms. Recent insights from network theory suggest that percolation phenomena, coupled with the dynamics of extracellular matrix crosslinking, play an important role in determining these divergent pathological trajectories. This review examines how critical percolation thresholds at which local damage or repair transitions to system-wide structural failure or rigidification determine the changes in lung tissue during chronic inflammation. We examine the mechanisms of collagen and elastin crosslinking, the feedback loops that amplify initial perturbations, and the threshold behaviors that push inflamed lung tissue toward either emphysematous destruction or fibrotic consolidation. Understanding these percolation-dependent transitions provides new insights into why similar inflammatory insults can produce opposite structural outcomes and suggests novel therapeutic strategies targeting the crosslinking mechanisms that underlie these critical transitions.

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Publication Details

Journal
Biomedicines
Published
2026-01-27
DOI
https://doi.org/10.3390/biomedicines14020281
Citations
1
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
36.44
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article

Percolation Forces in Lung Inflammation: Determining the Path to Emphysema or Fibrosis

Jerome Cantor
1 citations
Biomedicines
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
36.44
article

Percolation Forces in Lung Inflammation: Determining the Path to Emphysema or Fibrosis

Jerome Cantor
article en
1 citations

Abstract

The dichotomous outcomes of chronic lung inflammation, represented by either pulmonary emphysema or interstitial fibrosis, involve poorly understood overlapping mechanisms. Recent insights from network theory suggest that percolation phenomena, coupled with the dynamics of extracellular matrix crosslinking, play an important role in determining these divergent pathological trajectories. This review examines how critical percolation thresholds at which local damage or repair transitions to system-wide structural failure or rigidification determine the changes in lung tissue during chronic inflammation. We examine the mechanisms of collagen and elastin crosslinking, the feedback loops that amplify initial perturbations, and the threshold behaviors that push inflamed lung tissue toward either emphysematous destruction or fibrotic consolidation. Understanding these percolation-dependent transitions provides new insights into why similar inflammatory insults can produce opposite structural outcomes and suggests novel therapeutic strategies targeting the crosslinking mechanisms that underlie these critical transitions.

BiomedicinesVol. 14(2)
St. John's University (US)
Good health and well-being
Openalex Percentile: Top 1%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
36.44
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