Journal
THORAX
Volume 76, Issue 7, Pages 729-732Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/thoraxjnl-2020-215745
Keywords
COPD exacerbations; exercise; pulmonary rehabilitation
Categories
Funding
- NIH [R01 HL142265, R35 HL150767, R21 AG052744]
- Three Lakes Foundation
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The study found that EGCG can not only inhibit TGF beta 1 signaling and new collagen accumulation, but also activate matrix metalloproteinase-dependent collagen I turnover, suggesting the potential for slow fibrosis resolution with continued treatment.
We recently identified epigallocatechin gallate (EGCG), a trihydroxyphenolic compound, as a dual inhibitor of lysyl oxidase-like2 and transforming growth factor-beta 1 (TGF beta 1) receptor kinase that when given orally to patients with idiopathic pulmonary fibrosis (IPF) reversed profibrotic biomarkers in their diagnostic biopsies. Here, we extend these findings to advanced pulmonary fibrosis using cultured precision-cut lung slices from explants of patients with IPF undergoing transplantation. During these experiments, we were surprised to discover that not only did EGCG attenuate TGF beta 1 signalling and new collagen accumulation but also activated matrix metalloproteinase-dependent collagen I turnover, raising the possibility of slow fibrosis resolution with continued treatment.
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