GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver

Park, Sung Jin; Kim, Sanghwa; Kim, Min Jung; Hong, Youngeun; Lee, Ah Young; Lee, Hyunji; Tran, Quangdon; Kim, Minhee; Cho, Hyeonjeong; Park, Jisoo; Kim, Kwang Pyo; Park, Jongsun; Cho, Myung‐Haing

doi:10.1016/j.bbrc.2017.11.049

Cited by 25 publications

(18 citation statements)

References 32 publications

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“…ER stress can serve as a priming event to pulmonary fibrosis by affecting intracellular lipid events. For example, enhanced autophagy in Golgin A2 (GOLGA2) −/− mice limited the subcellular availability of functional mitochondria and lamellar bodies, and this was associated with decreased DPPC and a mild increase in extracellular matrix (ECM) deposition in both lungs and liver [147]. Intranasal tunicamycin increased ER stress, as well as expression of lipogenic enzymes fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1) and diglyceride acyltransferase (DGAT), their upstream regulator SREBP1, and intracellular triglyceride and PL content [148].…”

Section: Lipids In Interstitial Lung Disease and Idiopathic Pulmonarymentioning

confidence: 99%

Alveolar lipids in pulmonary disease. A review

2020

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Lung lipid metabolism participates both in infant and adult pulmonary disease. The lung is composed by multiple cell types with specialized functions and coordinately acting to meet specific physiologic requirements. The alveoli are the niche of the most active lipid metabolic cell in the lung, the type 2 cell (T2C). T2C synthesize surfactant lipids that are an absolute requirement for respiration, including dipalmitoylphosphatidylcholine. After its synthesis and secretion into the alveoli, surfactant is recycled by the T2C or degraded by the alveolar macrophages (AM). Surfactant biosynthesis and recycling is tightly regulated, and dysregulation of this pathway occurs in many pulmonary disease processes. Alveolar lipids can participate in the development of pulmonary disease from their extracellular location in the lumen of the alveoli, and from their intracellular location in T2C or AM. External insults like smoke and pollution can disturb surfactant homeostasis and result in either surfactant insufficiency or accumulation. But disruption of surfactant homeostasis is also observed in many chronic adult diseases, including chronic obstructive pulmonary disease (COPD), and others. Sustained damage to the T2C is one of the postulated causes of idiopathic pulmonary fibrosis (IPF), and surfactant homeostasis is disrupted during fibrotic conditions. Similarly, surfactant homeostasis is impacted during acute respiratory distress syndrome (ARDS) and infections. Bioactive lipids like eicosanoids and sphingolipids also participate in chronic lung disease and in respiratory infections. We review the most recent knowledge on alveolar lipids and their essential metabolic and signaling functions during homeostasis and during some of the most commonly observed pulmonary diseases.

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Section: Lipids In Interstitial Lung Disease and Idiopathic Pulmonarymentioning

confidence: 99%

Alveolar lipids in pulmonary disease. A review

2020

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“…It has been reported that the deletion of Golgin A2 (GOLGA2), encoding a cis-Golgi protein, induced the formation of the autophagosome via the releases of GABARAP from the Golgi 84 . Recently, researchers have revealed that the deletion of GOLGA2 induced autophagy and lung fibrosis by disrupting the Golgi function, increasing alveolar macrophages and reducing subcellular lipid storage in GOLGA2 KO mice 85 .…”

Section: Lung Fibrosis and Autophagymentioning

confidence: 99%

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Liu¹,

Wu²,

Li³

2020

Theranostics

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Fibrosis occurs in most human organs including the liver, lung, heart and kidney, and is crucial for the progression of most chronic diseases. As an indispensable catabolic process for intracellular quality control and homeostasis, autophagy occurs in most mammalian cells and is implicated in many biological processes including fibrogenesis. Although advances have been made in understanding autophagy process, the potential role of autophagy in fibrotic diseases remains controversial and has recently attracted a great deal of attention. In the current review, we summarize the commonalities of autophagy affecting different types of fibrosis in different organs, including the liver, lung, heart, and kidney as well as in cystic fibrosis, systematically outline the contradictory results and highlight the distinct role of autophagy during the various stages of fibrosis. In summary, the exact role autophagy plays in fibrogenesis depends on specific cell types and different stimuli, and identifying and evaluating the pathogenic contribution of autophagy in fibrogenesis will promote the discovery of novel therapeutic strategies for the clinical management of these fibrotic diseases.

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“…It has been demonstrated that autophagy can provide energy for HSC activation. A major feature of HSC activation is the release of lipid droplets containing retinol (vitamin A) and triglycerides, while autophagy can degrade lipid droplets in HSCs and hydrolyze the retinol into free fatty acids, which are further oxidized by mitochondria to produce ATP and provide energy for cell activation [ 60 – 62 ]. Inhibition of autophagy will reduce the degradation of lipid droplets, thereby preventing the activation of HSCs.…”

Section: The Role Of Nlrp3 Inflammasome and Autophagy In Liver Fibmentioning

confidence: 99%

The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis

Tao

Wang

Qiu

et al. 2020

BioMed Research International

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Liver fibrosis is an intrinsic repair process of chronic injury with excessive deposition of extracellular matrix. As an early stage of various liver diseases, liver fibrosis is a reversible pathological process. Therefore, if not being controlled in time, liver fibrosis will evolve into cirrhosis, liver failure, and liver cancer. It has been demonstrated that hepatic stellate cells (HSCs) play a crucial role in the formation of liver fibrosis. In particular, the activation of HSCs is a key step for liver fibrosis. Recent researches have suggested that autophagy and inflammasome have biological effect on HSC activation. Herein, we review current studies about the impact of autophagy and NOD-like receptors containing pyrin domain 3 (NLRP3) inflammasome on liver fibrosis and the underlying mechanisms.

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GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver

Cited by 25 publications

References 32 publications

Alveolar lipids in pulmonary disease. A review

Alveolar lipids in pulmonary disease. A review

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

The Role of Autophagy and NLRP3 Inflammasome in Liver Fibrosis

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