Mechanical Stretch: An Important and Understudied Feature of Acute and Chronic Lung Injury

Cagino, Leigh M.; Hensley, M.; Fortier, Sean M.; Dickson, Robert P.

doi:10.1164/rccm.201911-2166rr

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…In addition to the CS generated from the cardiac pulsatility, lung microvascular ECs are also subjected to CS as the result of respiration. As such, mechanical stretch would be a mechano stimulation during the onset of acute and chronic lung injury ( 34 ). The number of EPCs is significantly higher in patients with acute lung injury compared with healthy control subjects ( 35 ), suggesting that EPCs may participate in the lung repair after injury ( 36 ).…”

Section: Discussionmentioning

confidence: 99%

Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation

Han

Yan

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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Endothelial progenitor cells (EPCs) play an important role in vascular repair and re-endothelialization after vessel injury. EPCs in blood vessels are subjected to cyclic stretch (CS) due to the pulsatile pressure, but the role of CS in metabolic reprogramming of EPC, particularly its vascular homing and repair, is largely unknown. In the current study, physiological CS applied to EPCs at a magnitude of 10% and a frequency of 1 Hz significantly promoted their vascular adhesion and endothelial differentiation. CS enhanced mitochondrial elongation and oxidative phosphorylation (OXPHOS), as well as adenosine triphosphate production. Metabolomic study and Ultra-high performance liquid chromatography-mass spectrometry assay revealed that CS significantly decreased the content of long-chain fatty acids (LCFAs) and markedly induced long-chain fatty acyl-CoA synthetase 1 (Acsl1), which in turn facilitated the catabolism of LCFAs in mitochondria via fatty acid β-oxidation and OXPHOS. In a rat carotid artery injury model, transplantation of EPCs overexpressing Acsl1 enhanced the adhesion and re-endothelialization of EPCs in vivo. MRI and vascular morphology staining showed that Acsl1 overexpression in EPCs improved vascular repair and inhibited vascular stenosis. This study reveals a mechanotransduction mechanism by which physiological CS enhances endothelial repair via EPC patency.

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Section: Discussionmentioning

confidence: 99%

Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation

Han

Yan

et al. 2023

Proc. Natl. Acad. Sci. U.S.A.

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“…Interestingly collapse induration has been observed in patients with COVID-19 and is hypothesized to represent one of the initiating steps in the subsequent fibroproliferative response 121 , 122 , 123 . Mechanical stretching of alveolar spaces has also been demonstrated to directly activate pro-fibrotic signaling cascades and induced programmed cell death in type II AECs and may account for the peripheral distribution of fibrosis in IPF 124 , 125 , 126 . Hypoxia resultant from the mechanical distortion and collapse of alveolar spaces further compounds this injury and exacerbates pro-fibrotic responses 127 , 128 .…”

Section: Pathogenesis Of Ards-induced Fibrosismentioning

confidence: 99%

From ARDS to pulmonary fibrosis: the next phase of the COVID-19 pandemic?

Michalski

Kurche

Schwartz

2022

Translational Research

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While the coronavirus disease 19 (COVID-19) pandemic has transformed the medical and scientific communites since it was first reported in late 2019, we are only beginning to understand the chronic health burdens associated with this disease. Although COVID-19 is a multi-systemic disease, the lungs are the primary source of infection and injury, resulting in pneumonia and, in severe cases, acute respiratory distress syndrome (ARDS). Given that pulmonary fibrosis is a well-recognized sequela of ARDS, many have questioned whether COVID-19 survivors will face long-term pulmonary consequences. This review is aimed at integrating our understanding of the pathophysiologic mechanisms underlying fibroproliferative ARDS with our current knowledge of the pulmonary consequences of COVID-19 disease.

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Mechanical Stretch: An Important and Understudied Feature of Acute and Chronic Lung Injury

Cited by 2 publications

References 7 publications

Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation

Cyclic stretch promotes vascular homing of endothelial progenitor cells via Acsl1 regulation of mitochondrial fatty acid oxidation

From ARDS to pulmonary fibrosis: the next phase of the COVID-19 pandemic?

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