Inflammation and fibrosis

Mack, Matthias

doi:10.1016/j.matbio.2017.11.010

Cited by 352 publications

(292 citation statements)

References 245 publications

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“…Sterile inflammation and regeneration are two biological processes that are tightly related to wound healing, but if uncontrolled could lead to scarring and fibrotic responses, contributing to the long term to organ loss of function . Among cells involved in the modulation of these crucial functions, several types of macrophages play a central role in the clearance of dying/dead cells, and promote tissue repair by secreting a broad variety of molecules, such as cytokines, chemokines, or alarmins, that either maintain the inflammation process and/or activate tissue myofibroblasts in charge of synthesizing extracellular matrix components to promote tissue architecture restoration .…”

Section: Introductionmentioning

confidence: 99%

Macrophage‐derived HMGB1 is dispensable for tissue fibrogenesis

et al. 2019

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Alarmins and damage‐associated molecular patterns (DAMPs) are powerful inflammatory mediators, capable of initiating and maintaining sterile inflammation during acute or chronic tissue injury. Recent evidence suggests that alarmins/DAMPs may also trigger tissue regeneration and repair, suggesting a potential contribution to tissue fibrogenesis. High mobility group B1 (HMGB1), a bona fide alarmin/DAMP, may be released passively by necrotic cells or actively secreted by innate immune cells. Macrophages can release large amounts of HMGB1 and play a key role in wound healing and regeneration processes. Here, we hypothesized that macrophages may be a key source of HMGB1 and thereby contribute to wound healing and fibrogenesis. Surprisingly, cell‐specific deletion approaches, demonstrated that macrophage‐derived HMGB1 is not involved in tissue fibrogenesis in multiple organs with different underlying pathologies. Compared to control HMGB1Flox mice, mice with macrophage‐specific HMGB1 deletion (HMGB1ΔMac) do not display any modification of fibrogenesis in the liver after CCL4 or thioacetamide treatment and bile duct ligation; in the kidney following unilateral ureter obstruction; and in the heart after transverse aortic constriction. Of note, even under thermoneutral housing, known to exacerbate inflammation and fibrosis features, HMGB1ΔMac mice do not show impairment of fibrogenesis. In conclusion, our study clearly establishes that macrophage‐derived HMGB1 does not contribute to tissue repair and fibrogenesis.

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Section: Introductionmentioning

confidence: 99%

Macrophage‐derived HMGB1 is dispensable for tissue fibrogenesis

et al. 2019

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“…67 Prolonged inflammation and oxidative stress blocks the remodeling phase and promotes excessive fibrosis and scarring. [69][70][71] Therefore, stringent control of oxidative and inflammatory factors is important for the outcome of wound repair in skin and muscle. Several factors including the cytokines interleukin-1 beta (IL-1 β), interleukin-6 SCHREURS ET AL.…”

Section: Cleft Surgery Can Results In Fibrosis and Scar Formationmentioning

confidence: 99%

Tissue engineering strategies combining molecular targets against inflammation and fibrosis, and umbilical cord blood stem cells to improve hampered muscle and skin regeneration following cleft repair

Schreurs

Suttorp

Mutsaers

et al. 2019

Medicinal Research Reviews

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Cleft lip with or without cleft palate is a congenital deformity that occurs in about 1 of 700 newborns, affecting the dentition, bone, skin, muscles and mucosa in the orofacial region. A cleft can give rise to problems with maxillofacial growth, dental development, speech, and eating, and can also cause hearing impairment. Surgical repair of the lip may lead to impaired regeneration of muscle and skin, fibrosis, and scar formation. This may result in hampered facial growth and dental development affecting oral function and lip and nose esthetics. Therefore, secondary surgery to correct the scar is often indicated. We will discuss the molecular and cellular pathways involved in facial and lip myogenesis, muscle anatomy in the normal and cleft lip, and complications following surgery. The aim of this review is to outline a novel molecular and cellular strategy to improve musculature and skin regeneration and to reduce scar formation following cleft repair. Orofacial clefting can be diagnosed in the fetus through prenatal ultrasound screening and allows planning for the harvesting of umbilical cord blood stem cells upon birth. Tissue engineering techniques using these cord blood stem cells and molecular targeting of inflammation and fibrosis during surgery may promote tissue regeneration. We expect that this novel strategy improves both muscle and skin regeneration, resulting in better function and esthetics after cleft repair.

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“…In the injured liver chemotactic stimuli trigger the rapid recruitment of immune cells including macrophages and neutrophils. These infiltrating immune cells then produce numerous proinflammatory cytokines and growth factors, which trigger the activation of myofibroblasts, the main effector cells of tissue remodeling [32]. Accordingly, there are reasons to believe that the increase in circulating PTX3 levels is likely triggered by ongoing production of proinflammatory cytokines at necroinflammatory injury, including IL-1 and TNF-, which are known to be potent inducers of PTX3 release [33].…”

Section: Discussionmentioning

confidence: 99%

“…Thirdly, major strength of the study is the comparison to FibroScan5 as this novel elastography technique fulfills a number of the requirements of an ideal noninvasive marker of fibrosis. However, FibroScan5 has some limitations such as the lack of standardized cut-off for diagnosing fibrosis stages [32]. Because we relied on a single determination of PTX3, we cannot take into account any variation that may have occurred over time.…”

Section: Discussionmentioning

confidence: 99%

Pentraxin 3 Detects Clinically Significant Fibrosis in Patients with Chronic Viral Hepatitis C

Górka-Dynysiewicz

Pazgan−Simon

Zuwała−Jagiełło

2019

BioMed Research International

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Pentraxin 3 (PTX3) plays a pathogenic role in experimental models of chronic liver injury and contributes to the progression of fibrosis. The detection of advanced fibrosis (METAVIR F≥3) is important to identify patients who are in urgent need of antiviral treatments versus those whose treatment could be deferred (F≥2). The aim was to assess the diagnostic value of PTX3 as a potential biomarker for clinically significant and advanced fibrosis. PTX3 associations with biochemical and histological parameters of inflammatory activity and fibrosis were investigated in 138 patients with chronic viral hepatitis C (HCV) before antiviral treatment. METAVIR histological scores of activity and fibrosis were obtained. PTX3 was measured by enzyme-linked immunosorbent assay. The diagnostic accuracy of serum PTX3 levels was compared to that of other fibrosis markers, including transforming growth factor‐β1 (TGF-β1), hyaluronic acid (HA), aspartate transaminase to platelet ratio index (APRI), fibrosis score based on four factors (FIB4), gamma-glutamyltranspeptidase to platelet ratio (GPR), and the liver stiffness measurement (LSM) by transient elastography (FibroScan®). In HCV patients the PTX3 level increased in parallel with the METAVIR histological score of activity, being independently associated with the METAVIR fibrosis score (P < 0.001). Using the receiver operating characteristics analysis, the best marker for detecting F≥2 and F≥3 was PTX3 with AUC = 0.802 and AUC = 0.867, respectively. The area under the curve of PTX3 for predicting significant fibrosis (F≥2) was significantly greater than those for the GPR ratio (AUC = 0.648) and FIB-4 score (AUC = 0.770) and similar to that for APRI index (AUC = 0.831). PTX3 provided clinically relevant diagnostic accuracy as a single marker of significant fibrosis.

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Inflammation and fibrosis

Cited by 352 publications

References 245 publications

Macrophage‐derived HMGB1 is dispensable for tissue fibrogenesis

Macrophage‐derived HMGB1 is dispensable for tissue fibrogenesis

Tissue engineering strategies combining molecular targets against inflammation and fibrosis, and umbilical cord blood stem cells to improve hampered muscle and skin regeneration following cleft repair

Pentraxin 3 Detects Clinically Significant Fibrosis in Patients with Chronic Viral Hepatitis C

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