Shared and distinct mechanisms of fibrosis

Distler, Jörg H W; Györfi, Andrea-Hermina; Ramanujam, Meera; Whitfield, Michael L.; Königshoff, Mélanie; Lafyatis, Robert

doi:10.1038/s41584-019-0322-7

Cited by 425 publications

(399 citation statements)

References 390 publications

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“…Fibrosis results from an abnormal healing process coupled with an aberrant expansion of mesenchymal cells that originate from multiple sources including: bone marrow, the transdifferentiation of pericytes, epithelial cells and endothelial cells, and the differentiation from resident fibroblasts to myofibroblasts [16,18]. Transforming growth factor-beta is thought to play a central role in the development and progression of fibrosis in SSc-ILD [6,16] and platelet-derived growth factor, Wnt-βcatenin and hedgehog signalling also drive fibrosis [18,19]. SSc fibroblasts have been shown to be more resistant to the fibrotic-inhibitory potential of cytokines, such as interferon gamma [20].…”

Section: Pathogenesis Of Ssc-ildmentioning

confidence: 99%

Predictors of progression in systemic sclerosis patients with interstitial lung disease

Assassi²,

et al. 2020

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Systemic sclerosis (SSc) is a systemic autoimmune disease affecting multiple organ systems, including the lungs. Interstitial lung disease (ILD) is the leading cause of death in SSc.There are no valid biomarkers to predict the occurrence of SSc-ILD, although auto-antibodies against anti-topoisomerase I and several inflammatory markers are candidate biomarkers that need further evaluation. Chest auscultation, presence of shortness of breath and pulmonary function testing are important diagnostic tools, but lack sensitivity to detect early ILD. Baseline screening with high-resolution computed tomography (HRCT) is therefore necessary to confirm an SSc-ILD diagnosis. Once diagnosed with SSc-ILD, patients' clinical courses are variable and difficult to predict, although certain patient characteristics and biomarkers are associated with disease progression. It is important to monitor patients with SSc-ILD for signs of disease progression, although there is no consensus about which diagnostic tools to use or how often monitoring should occur. In this article, we review methods used to define and predict disease progression in SSc-ILD.There is no valid definition of SSc-ILD disease progression, but we suggest that either a decline in forced vital capacity (FVC) from baseline of ≥10%, or a decline in FVC of 5–9% in association with a decline in diffusing capacity of the lung for carbon monoxide of ≥15% represents progression. An increase in the radiographic extent of ILD on HRCT imaging would also signify progression. A time period of 1–2 years is generally used for this definition, but a decline over a longer time period may also reflect clinically relevant disease progression.

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Section: Pathogenesis Of Ssc-ildmentioning

confidence: 99%

Predictors of progression in systemic sclerosis patients with interstitial lung disease

Assassi²,

et al. 2020

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“…Fibrosis is a process characterized by excessive deposits of extracellular matrix that leads to the replacement of functional parenchyma by fibrotic tissue [22]. Renal fibrosis is the common pathological process in chronic kidney disease, despite the underlying cause, in which kidney gradually lost its ability to repair as a result of ongoing tissue injury and inflammation [23].…”

Section: Macrophage Phenotype and Fibrosismentioning

confidence: 99%

Macrophage Phenotype and Fibrosis in Diabetic Nephropathy

Calle

Hotter

2020

IJMS

149

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Diabetic nephropathy (DN) is the leading cause of end-stage renal disease globally. The primary initiating mechanism in DN is hyperglycemia-induced vascular dysfunction, but its progression is due to different pathological mechanisms, including oxidative stress, inflammatory cells infiltration, inflammation and fibrosis. Macrophages (Mφ) accumulation in kidneys correlates strongly with serum creatinine, interstitial myofibroblast accumulation and interstitial fibrosis scores. However, whether or not Mφ polarization is involved in the progression of DN has not been adequately defined. The prevalence of the different phenotypes during the course of DN, the existence of hybrid phenotypes and the plasticity of these cells depending of the environment have led to inconclusive results. In the same sense the role of the different macrophage phenotype in fibrosis associated or not to DN warrants additional investigation into Mφ polarization and its role in fibrosis. Due to the association between fibrosis and the progressive decline of renal function in DN, and the role of the different phenotypes of Mφ in fibrosis, in this review we examine the role of macrophage phenotype control in DN and highlight the potential factors contributing to phenotype change and injury or repair in DN.

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“…The Wnt/β-catenin signal transduction pathway is essential for adult life of human beings, and could control myriad biological phenomena throughout development [6]. The Wnt signal also plays an essential role in brotic disease, and inhibiting this pathway could effectively suppress the brotic progression [7].…”

Section: Introductionmentioning

confidence: 99%

Ellagic Acid Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting Wnt Signaling Pathway

Huang

Liu

et al. 2020

Preprint

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Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with high mortality, which characterized by epithelial cell damage and fibroblasts activation. Ellagic acid (EA) is a natural polyphenol compound widely found in fruits and nuts which has demonstrated multiple pharmacological activities. Herein we showed that Ellagic acid significantly alleviated bleomycin(BLM)-induced pulmonary fibrosis in mice, and also inhibited the Wnt/β-catenin signal in primary pulmonary fibroblasts. In vitro experiments indicated that Ellagic acid apparently suppressed Wnt3a-induced myofibroblasts activation and ECM accumulation mainly via inhibiting the phosphorylation of Erk2 and Akt. Further studies showed that Ellagic acid could induce autophagy formation of myofibroblasts mainly by suppressing mTOR signaling and promote apoptosis of myofibroblasts. In vivo experiments reveled that Ellagic acid significantly inhibited myofibroblasts activation and promoted autophagy formation. Taken together, our results showed that Ellagic acid effectively attenuated BLM-induced pulmonary fibrosis in mice by suppressing myofibroblasts activation, promoting autophagy and apoptosis of myofibroblasts mainly via inhibiting Wnt signaling pathway.

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Shared and distinct mechanisms of fibrosis

Cited by 425 publications

References 390 publications

Predictors of progression in systemic sclerosis patients with interstitial lung disease

Predictors of progression in systemic sclerosis patients with interstitial lung disease

Macrophage Phenotype and Fibrosis in Diabetic Nephropathy

Ellagic Acid Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting Wnt Signaling Pathway

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