Common and unique mechanisms regulate fibrosis in various fibroproliferative diseases.

By TA Wynn. Journal of Clinical Investigation, 2007

1,450 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/733760f0a9d503235f5392075ae915c37fc66358

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Citations in the corpus

Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “The CC chemokines macrophage inflammatory protein (MIP)-1a, MIP-1b, and regulated upon activation, normal t-cell expressed and secreted (RANTES), together with their corresponding receptors CCR1 and CCR5, are also routinely up-regulated in models of liver fibrogenesis.(25) Furthermore, neutralizatio”
Cellular and molecular mechanisms of fibrosis (2008, background): “Despite having distinct aetiological and clinical manifestations, most chronic fibrotic disorders have in common a persistent irritant that sustains the production of growth factors, proteolytic enzymes, angiogenic factors and fibrogenic cytokines, which stimulate the deposition of connective tissue”
Fibrosis and Adipose Tissue Dysfunction (2013, background): “The accumulation of fibrosis is the culmination of several pathological processes and can affect different organs, such as the liver, heart, and kidney (Wynn, 2007).”
Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis (2009, background): “Arg1 downregulates chronic inflammation Although chronic inflammation typically contributes to tissue remodeling and fibrosis, recent studies have suggested that the mechanisms controlling inflammation and fibrosis are distinct [20].”
TGF-β1 Signaling and Tissue Fibrosis. (2018, background): “Collectively, fibrosis is a leading cause of death and morbidity in the developed world, accounting for up to 45% of all deaths by some estimates (Wynn 2007).”
PAI-1 in Tissue Fibrosis (2012, background): “Although the etiology of fibrosis in different organs is not properly defined, numerous studies suggest that at the molecular level, fibrogenic processes in different organs may share common mechanisms (Wynn, 2007, 2008; Ghosh, 2010).”
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis (2010, background): “Fibroblastic foci are aggregations of fibroblasts/myofibroblasts that produce excessive ECM components (Wynn, 2007; Hardie et al., 2009).”
Integrating mechanisms of pulmonary fibrosis (2011, background): “Repair of damaged tissues is a fundamental biological mechanism that allows the ordered replacement of dead or damaged cells after injury, a process critically important for survival (Wynn, 2007).”
The extracellular matrix: an active or passive player in fibrosis? (2011, background): “Fibrosis can be viewed as the result of a series of ECM changes that take place over time (9, 72).”
The IL-33/ST2 pathway: therapeutic target and novel biomarker (2008, background): “Involvement of sST2 in TLR-4 signalling had been suggested previously, in the model of LPS-induced sepsis as mentioned belo”
Hepatic fibrosis: Concept to treatment. (2015, background): “The ECM also functions as a reservoir for pro-inflammatory and pro-fibrogenic mediators [4].”
Cellular and molecular mechanisms of renal fibrosis (2011, background): “Even αSMA, a classic marker of myofibroblast activation in organ fibrosis of all types”
Therapy for Fibrotic Diseases: Nearing the Starting Line (2013, background): “Many of these targets are also affected in other fibrotic diseases of kidney, as well as in other tissues, revealing stereotypical transcriptional changes for the inciting injury across several organs (3, 180).”
Remodeling and homeostasis of the extracellular matrix: implications for fibrotic diseases and cancer (2011, neutral): “Consequently, even sophisticated 3D in vitro models might not represent the physiological conditions found in vivo (Schmeichel and Bissell, 2003; Pampaloni et al., 2007; Yamada and Cukierman, 2007).”