The role of macrophage–fibroblast interaction in lipopolysaccharide-induced pulmonary fibrosis: an acceleration in lung fibroblast aerobic glycolysis

Xu, Qiaoyi; Mei, Shuya; Nie, Fang; Zhang, Zhiyun; Feng, Junqi; Zhang, Jinyuan; Qian, Xiaoqing; Gao, Yuan; He, Zhengyu; Xing, Shunpeng

doi:10.1038/s41374-021-00701-7

Cited by 21 publications

(12 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Local factors throughout the body shape the tissue-specific phenotypes of both macrophages and fibroblasts during steady state and inflammation. These include changes in the local concentration of various metabolites such as retinoic acid or lactate as well as variations in oxygen tension that impact both on the local pool of macrophages and fibroblasts ( 90 , 91 ). Also, the presence of unique factors that shape the specific microenvironmental niche such as surfactant in the lung, bacteria in the gut or synovial fluid within the joints likely imprint on the phenotypic features of both cell types.…”

Section: Crosstalk Between Synovial Fibroblasts and Macrophagesmentioning

confidence: 99%

“…This homeostatic equilibrium and balanced interaction might become disturbed during various disease states where macrophages and/or fibroblast activity is altered and consequently affects the other cell type. Excessive production of cytokines such as IL-6 and of chemokines such as CCL2 by fibroblasts or increased secretion of TGFbeta and PDGF by macrophages might be the consequence thereby contributing to excessive inflammation and/or a fibrotic reaction Such pathologic circuits have been described to contribute to diseases such as lung fibrosis, but might well be involved in synovial inflammation and synovial pannus formation during RA as well ( 90 , 96 ). Cellular communication between macrophages and fibroblasts seem to partially amplify both a pro-fibrotic response in fibroblasts and a pro-inflammatory response in macrophages, thereby driving a vicious circle of TGFbeta production by macrophages and IL-6 production by fibroblasts ( 97 , 98 ).…”

Section: Crosstalk Between Synovial Fibroblasts and Macrophagesmentioning

confidence: 99%

See 1 more Smart Citation

Synovial Macrophage and Fibroblast Heterogeneity in Joint Homeostasis and Inflammation

2022

View full text Add to dashboard Cite

The synovial tissue is an immunologically challenging environment where, under homeostatic conditions, highly specialized subsets of immune-regulatory macrophages and fibroblasts constantly prevent synovial inflammation in response to cartilage- and synovial fluid-derived danger signals that accumulate in response to mechanical stress. During inflammatory joint diseases, this immune-regulatory environment becomes perturbed and activated synovial fibroblasts and infiltrating immune cells start to contribute to synovial inflammation and joint destruction. This review summarizes our current understanding of the phenotypic and molecular characteristics of resident synovial macrophages and fibroblasts and highlights their crosstalk during joint homeostasis and joint inflammation, which is increasingly appreciated as vital to understand the molecular basis of prevalent inflammatory joint diseases such as rheumatoid arthritis.

show abstract

Section: Crosstalk Between Synovial Fibroblasts and Macrophagesmentioning

confidence: 99%

Section: Crosstalk Between Synovial Fibroblasts and Macrophagesmentioning

confidence: 99%

Synovial Macrophage and Fibroblast Heterogeneity in Joint Homeostasis and Inflammation

2022

View full text Add to dashboard Cite

show abstract

“…An allosteric activator of phosphofructokinase-1, 6-phosphofructo-2-kinase/fructose-2,6- biphosphatase 3 (PFKFB3) is also upregulated in Transforming growth factor-β (TGF-β)-induced myofibroblasts, and the inhibition of PFKFB3 effectively decreases levels of myofibroblasts differentiation and pulmonary fibrosis ( Xie et al, 2015 ). PFKFB3 expression can be increased by the secretion of TNF-α in lung fibroblasts, while PFKFB3 suppression effectively blocks TNF-α-induced aerobic glycolysis and lactate production in fibroblasts ( Xu et al, 2022 ). The anti-fibrotic effect of Anlotinib is demonstrated to inhibit PFKFB3-dependent glycolysis, which can be post-transcriptionally regulated by the RNA-binding protein PCBP3 ( Chen et al, 2021 ).…”

Section: Myofibroblastsmentioning

confidence: 99%

Metabolic reprogramming of pulmonary fibrosis

Zhai²,

Sun³

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

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.

show abstract

“…As evident, acute lung injury can also lead to pulmonary brosis as a result of infection or any physical or chemical trauma [65]. In rat model, Ye et al, nd ten differentially expressed circRNAs in BAL and tissue samples after smoke inhalation, indicating that circRNAs have an apparent role in smoke induced ALI and pulmonary brosis [66].…”

Section: Circular Rnasmentioning

confidence: 99%

Non-Coding RNA in Idiopathic Interstitial Pneumonia and Covid-19 Pulmonary Fibrosis

Ali

Singh

Alam

et al. 2022

Preprint

View full text Add to dashboard Cite

Pulmonary fibrosis is the major manifestation of idiopathic interstitial pneumonia as well as post-COVID-19 complications. The pathogenesis of PF is a complex molecular process that involves many types of cells, proteins, genes, and regulatory elements. The non-coding RNA is the main regulatory element in this process which mainly includes; miRNA, circRNA, and lncRNA. These regulatory elements control the expression of many important genes and various pathways that are involved in the pathogenesis of pulmonary fibrosis. Identification and molecular mechanisms by which these non-coding RNA molecules works are very important because they do not only help to understand the molecular basis of the disease but could also serve as a potential diagnostic/prognostic marker as well as therapeutic targets. In this review, we have provided the latest findings and discussed the role of these regulatory elements in various biological processes and pathways involved in the pathogenesis of pulmonary fibrosis associated with IIPs and Covid-19.

show abstract

The role of macrophage–fibroblast interaction in lipopolysaccharide-induced pulmonary fibrosis: an acceleration in lung fibroblast aerobic glycolysis

Cited by 21 publications

References 22 publications

Synovial Macrophage and Fibroblast Heterogeneity in Joint Homeostasis and Inflammation

Synovial Macrophage and Fibroblast Heterogeneity in Joint Homeostasis and Inflammation

Metabolic reprogramming of pulmonary fibrosis

Non-Coding RNA in Idiopathic Interstitial Pneumonia and Covid-19 Pulmonary Fibrosis

Contact Info

Product

Resources

About