Preventing Glutaminolysis: A Potential Therapy for Pulmonary Fibrosis

Esguerra, Vincent; Zhao, Yutong

doi:10.1165/rcmb.2019-0119ed

Cited by 6 publications

(2 citation statements)

References 12 publications

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“…TGF-β1 induces GLS1 expression via SMAD3 and p38-MAPK-dependent signaling pathways, which are accompanied by enhanced levels of glutaminolysis in myofibroblasts. The GLS1 inhibitor, CB-839, exerts a protective effect in mice exposed to bleomycin or adenovirus expressing active TGF-β1 ( Bernard et al, 2018 ; Esguerra and Zhao, 2019 ). Additionally, PPAR-γ is a regulator of GLS1-mediated glutaminolysis ( Genovese et al, 2005 ).…”

Section: Myofibroblastsmentioning

confidence: 99%

Metabolic reprogramming of pulmonary fibrosis

Zhai²,

Sun³

et al. 2022

Front. Pharmacol.

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Pulmonary fibrosis is a progressive and intractable lung disease with fibrotic features that affects alveoli elasticity, which leading to higher rates of hospitalization and mortality worldwide. Pulmonary fibrosis is initiated by repetitive localized micro-damages of the alveolar epithelium, which subsequently triggers aberrant epithelial-fibroblast communication and myofibroblasts production in the extracellular matrix, resulting in massive extracellular matrix accumulation and interstitial remodeling. The major cell types responsible for pulmonary fibrosis are myofibroblasts, alveolar epithelial cells, macrophages, and endothelial cells. Recent studies have demonstrated that metabolic reprogramming or dysregulation of these cells exerts their profibrotic role via affecting pathological mechanisms such as autophagy, apoptosis, aging, and inflammatory responses, which ultimately contributes to the development of pulmonary fibrosis. This review summarizes recent findings on metabolic reprogramming that occur in the aforementioned cells during pulmonary fibrosis, especially those associated with glucose, lipid, and amino acid metabolism, with the aim of identifying novel treatment targets for pulmonary fibrosis.

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Section: Myofibroblastsmentioning

confidence: 99%

Metabolic reprogramming of pulmonary fibrosis

Zhai²,

Sun³

et al. 2022

Front. Pharmacol.

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“…Otherwise, it is unknown whether other anaplerotic pathways, such as those that are dependent on PCK1, which is known to be coordinated with GLS-1 upregulation, can also contribute to liver fibrosis in a paracrine manner, besides its role in the MFBs phenotype maintenance [ 102 , 103 ]. Still, these data highlight the necessity to include glutaminolysis and its intermediate metabolites as potential targets to consider for liver antifibrogenic therapies, such as those already suggested in fibrosis of other tissues [ 104 ].…”

Section: Metabolic Reprogramming Of Hsc In Fibrogenesismentioning

confidence: 99%

Metabolic Reprogramming of Liver Fibrosis

Delgado

Cárdenas

Farran

et al. 2021

Cells

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Liver fibrosis is an excessive and imbalanced deposition of fibrous extracellular matrix (ECM) that is associated with the hepatic wound-healing response. It is also the common mechanism that contributes to the impairment of the liver function that is observed in many chronic liver diseases (CLD). Despite the efforts, no effective therapy against fibrosis exists yet. Worryingly, due to the growing obesity pandemic, fibrosis incidence is on the rise. Here, we aim to summarize the main components and mechanisms involved in the progression of liver fibrosis, with special focus on the metabolic regulation of key effectors of fibrogenesis, hepatic stellate cells (HSCs), and their role in the disease progression. Hepatic cells that undergo metabolic reprogramming require a tightly controlled, fine-tuned cellular response, allowing them to meet their energetic demands without affecting cellular integrity. Here, we aim to discuss the role of ribonucleic acid (RNA)-binding proteins (RBPs), whose dynamic nature being context- and stimuli-dependent make them very suitable for the fibrotic situation. Thus, we will not only summarize the up-to-date literature on the metabolic regulation of HSCs in liver fibrosis, but also on the RBP-dependent post-transcriptional regulation of this metabolic switch that results in such important consequences for the progression of fibrosis and CLD.

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Ambient PM2.5 orchestrates M1 polarization of alveolar macrophages via activating glutaminase 1-mediated glutaminolysis in acute lung injury

Su,

Tu,

et al. 2025

Environmental Pollution

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Preventing Glutaminolysis: A Potential Therapy for Pulmonary Fibrosis

Cited by 6 publications

References 12 publications

Metabolic reprogramming of pulmonary fibrosis

Metabolic reprogramming of pulmonary fibrosis

Metabolic Reprogramming of Liver Fibrosis

Ambient PM2.5 orchestrates M1 polarization of alveolar macrophages via activating glutaminase 1-mediated glutaminolysis in acute lung injury

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