ArticlebioRxiv : the preprint server for biology2026
Mechanosignaling promotes macrophage apoptosis resistance in pulmonary fibrosis
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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18 authors.
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Abstract
The mechanisms underlying disease progression in idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases remain unclear. Increased extracellular matrix stiffness is a hallmark of fibrotic lung diseases, while monocyte-derived macrophages promote fibrosis progression. However, there is limited understanding if mechanical properties of the fibrotic microenvironment influence macrophage phenotypes and fibrogenesis. Profibrotic macrophages are resistant to apoptosis, which is modulated by enhanced mitochondrial bioenergetics. The objective of this study is to determine how lung tissue stiffness impacts macrophage phenotypes and fibrotic progression. We demonstrate that mechanoactivated macrophages exhibit apoptosis-resistance, increased expression of the antiapoptotic protein Bcl-xL, and elevated mitochondrial oxidative phosphorylation. Critically, the metabolic reprogramming observed in mechanoactivated macrophages is dependent on increased glutaminolysis. Inhibition of glutaminolysis attenuated apoptosis resistance in mechanoactivated macrophages. Moreover, inhibition of Bcl-xL
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