Normal lung development needs self-eating

Warburton, David; Bellusci, Saverio

doi:10.1172/jci129442

Cited by 7 publications

(3 citation statements)

References 19 publications

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“…acute respiratory distress syndrome (ARDS) (537), has recently been described to be an important regulator of lung development and, if deregulated, might contribute to BPD (620,646). Autophagy has been described to be induced by hyperoxia in rodent models of BPD (318,674), together with necroptosis (194,563).…”

Section: Autophagy Necroptosis Apoptosis and Senescencementioning

confidence: 99%

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Lignelli

Palumbo

Myti

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

111

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Bronchopulmonary dysplasia (BPD) is the most common cause of morbidity and mortality in preterm infants. A key histopathological feature of BPD is stunted late lung development, where the process of alveolarization—the generation of alveolar gas exchange units—is impeded, through mechanisms that remain largely unclear. As such, there is interest in the clarification both of the pathomechanisms at play in affected lungs, and the mechanisms of de novo alveoli generation in healthy, developing lungs. A better understanding of normal and pathological alveolarization might reveal opportunities for improved medical management of affected infants. Furthermore, disturbances to the alveolar architecture are a key histopathological feature of several adult chronic lung diseases, including emphysema and fibrosis, and it is envisaged that knowledge about the mechanisms of alveologenesis might facilitate regeneration of healthy lung parenchyma in affected patients. To this end, recent efforts have interrogated clinical data, developed new—and refined existing—in vivo and in vitro models of BPD, have applied new microscopic and radiographic approaches, and have developed advanced cell-culture approaches, including organoid generation. Advances have also been made in the development of other methodologies, including single-cell analysis, metabolomics, lipidomics, and proteomics, as well as the generation and use of complex mouse genetics tools. The objective of this review is to present advances made in our understanding of the mechanisms of lung alveolarization and BPD over the period 1 January 2017–30 June 2019, a period that spans the 50th anniversary of the original clinical description of BPD in preterm infants.

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Section: Autophagy Necroptosis Apoptosis and Senescencementioning

confidence: 99%

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Lignelli

Palumbo

Myti

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

111

View full text Add to dashboard Cite

show abstract

“…Previous investigations have demonstrated the crucial role of autophagy in normal lung development and morphogenesis. 4 , 5 Conversely, autophagy is substantially impaired in the lung tissues of BPD animal models. 6 However, the introduction of an autophagy activator has been shown to effectively ameliorate apoptosis and restored impaired alveolar development in hyperoxia-induced BPD models using Sprague–Dawley (SD) pups.…”

Section: Introductionmentioning

confidence: 99%

Tat-P combined with GAPR1 releases Beclin1 to promote autophagy and improve Bronchopulmonary dysplasia model

Zhou,

Zhu,

Jin

et al. 2023

iScience

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“…7 Relevant studies have shown that autophagy plays an important role in lung injury induced by hyperoxia, but it is mainly concentrated in the alveoli. [8][9][10] In fact, there is also a close link between autophagy and vascular damage. 11 In a mouse model of hindlimb ischemia, ischemia induces autophagy in endothelial cells and stimulates angiogenesis.…”

mentioning

confidence: 99%

Protective Effect and Mechanism of Autophagy in Endothelial Cell Injury Induced by Hyperoxia

Zhu,

He,

Zhang

et al. 2023

Am J Perinatol

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Objective Bronchopulmonary dysplasia is a chronic lung disease in premature infants with alveolar simplification and pulmonary vascular development disorder as the main pathological feature and hyperoxia as the main etiology. Autophagy is a highly conserved cytological behavior of self-degrading cellular components and is accompanied by oxidative stress. Studies have reported that autophagy is regulated by FOXO1 posttranslational modification. However, whether autophagy can be involved in the regulation of endothelial cell injury induced by hyperoxia and its mechanism are still unclear. Study Design We have activated and inhibited autophagy in human umbilical vein endothelial cells under hyperoxia and verified the role of autophagy in endothelial cell-related functions from both positive and negative aspects. Results Our research showed that the expression level of autophagy-related proteins decreased, accompanied by decreased cell migration ability and tube formation ability and increased cell reactive oxygen species level and cell permeability under hyperoxia conditions. Using an autophagy agonist alleviated hyperoxia-induced changes and played a protective role. However, inhibition of autophagy aggravated the cell damage induced by hyperoxia. Moreover, the decrease in autophagy proteins was accompanied by the upregulation of FOXO1 phosphorylation and acetylation. Conclusion We concluded that autophagy was a protective mechanism against endothelial cell injury caused by hyperoxia. Autophagy might participate in this process by coregulating posttranslational modifications of FOXO1. Key Points

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Normal lung development needs self-eating

Cited by 7 publications

References 19 publications

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia

Tat-P combined with GAPR1 releases Beclin1 to promote autophagy and improve Bronchopulmonary dysplasia model

Protective Effect and Mechanism of Autophagy in Endothelial Cell Injury Induced by Hyperoxia

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