Mechanisms of fibrosis: therapeutic translation for fibrotic disease
By TA Wynn, T. Ramalingam. Nature Medicine, 2012
3,308 citations recorded by the source corpus.
Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix–producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.
Subfields: Pathology and Forensic Medicine, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/404f03060e7d55e1c8e46a36e908dc5bfcefd4da
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In Pathology and Forensic Medicine
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Macrophage plasticity, polarization, and function in health and disease (2018, background): “…in the recovery phase of fibrosis by inducing ECM degradation, phagocytosis apoptotic myofibroblasts, and dampening the immune response that contributes to tissue injury (Braga et al., 2015; Sica et al., 2014; Tacke & Zimmermann, 2014;Wick et al., 2010; Wynn & Ramalingam, 2012; Xu et al., 2012).”
- Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease (2012, background): “Myocardial fibrosis in response to cardiac pressure overload is a characteristic feature of this disease and has been reported to result from proliferation of resident CFBs [39] as well as transformation of endothelial cells to mesenchymal cells leading to generation of CFBs and myoFBs [40,41].”
- TGF-β/Smad signaling in renal fibrosis (2015, background): “Emerging evidence suggests that the accumulation of myofibroblasts, a predominant source for ECM production, is a critical step in the progression of renal fibrosis (Wynn and Ramalingam, 2012).”
- Three-Dimensional in Vitro Cell Culture Models in Drug Discovery and Drug Repositioning (2018, background): “…growth factors and ECMproteins play significant roles in the development of fibrotic diseases in many tissues including liver, lung and kidney (Wynn and Ramalingam, 2012; Bonnans et al., 2014; Handorf et al., 2015), requiring genuine culture models that can mimic in vivo conditions for such…”
- Myocardial T1 mapping and extracellular volume quantification: a Society for Cardiovascular Magnetic Resonance (SCMR) and CMR Working Group of the European Society of Cardiology consensus statement (2013, background): “just like other organs, fibrosis in the myocardium is associated with cardiac dysfunction [38].”
- The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017, neutral): “Concomitantly, activated myofibroblasts in the area secrete collagen to maintain the integrity of the damaged tissue (65).”
- Wound repair and regeneration: Mechanisms, signaling, and translation (2014, neutral): “Novel therapies for the treatment of cutaneous pathological scarring may be extrapolated from clinical trials targeting fibrosis in other organs including lung, liver, or kidney (18).”