Myofibroblast

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Fibroblasts are cells present throughout the human body that are primarily responsible for the production and maintenance of the extracellular matrix ECM within the tissues. They have the capability to modify the mechanical properties of the ECM within the tissue and transition into myofibroblasts, a cell type that is associated with the development of fibrotic tissue through an acute increase of cell density and protein deposition. This transition from fibroblast to myofibroblast—a well-known cellular hallmark of the pathological state of tissues—and the environmental stimuli that can induce this transition have received a lot of attention, for example in the contexts of asthma and cardiac fibrosis. Recent efforts in understanding how cells sense their physical environment at the micro- and nano-scales have ushered in a new appreciation that the substrates on which the cells adhere provide not only passive influence, but also active stimulus that can affect fibroblast activation. These studies suggest that mechanical interactions at the cell—substrate interface play a key role in regulating this phenotype transition by changing the mechanical and morphological properties of the cells.

Myofibroblast

Federal government websites often end in. The site is secure. No new data were created or analysed in this study. Data sharing is not applicable to this article. Myofibroblasts mediate wound contractions, but their persistent presence in tissues is central to driving fibrosis, making them attractive cell targets for the development of therapeutic treatments. However, due to shared cellular markers with several other phenotypes, the specific targeting of myofibroblasts has long presented a scientific and clinical challenge. In recent years, myofibroblasts have drawn much attention among scientific research communities from multiple disciplines and specialisations. As further research uncovers the characterisations of myofibroblast formation, function, and regulation, the realisation of novel interventional routes for myofibroblasts within pathologies has emerged. The research community is approaching the means to finally target these cells, to prevent fibrosis, accelerate scarless wound healing, and attenuate associated disease-processes in clinical settings. This comprehensive review article describes the myofibroblast cell phenotype, their origins, and their diverse physiological and pathological functionality. Special attention has been given to mechanisms and molecular pathways governing myofibroblast differentiation, and updates in molecular interventions.

The shared features of the abnormal and excessive accumulation of ECM constituents, particularly collagens, HA, and FN, in these diseases are governed by myofibroblast myofibroblast phenotype, myofibroblast. The accompanying poster summarizes central aspects of myofibroblast biology for newcomers but also aims to entertain those skilled in myofibroblast myofibroblast art. Poster Panel 2 - jpeg file.

J Cell Sci 1 July ; 13 : jcs Now, myofibroblasts are not only recognized for their physiological role in tissue repair but also as cells that are key in promoting the development of fibrosis in all organs. In this Cell Science at a Glance and the accompanying poster, we provide an overview of the current understanding of central aspects of myofibroblast biology, such as their definition, activation from different precursors, the involved signaling pathways and most widely used models to study their function. Myofibroblasts will be placed into context with their extracellular matrix and with other cell types communicating in the fibrotic environment. Furthermore, the challenges and strategies to target myofibroblasts in anti-fibrotic therapies are summarized to emphasize their crucial role in disease progression. Myofibroblasts have crucial physiological roles in rapidly repairing injured tissues by laying down collagen scar, like in skin after trauma or heart after cardiac infarction. In addition, myofibroblasts are key effector cells in almost all organ fibrosis by persistently accumulating and contracting scar tissue beyond normal repair Hinz, a ; Horowitz and Thannickal,

Cell Communication and Signaling volume 22 , Article number: Cite this article. Metrics details. Pulmonary fibrosis PF is a progressive interstitial inflammatory disease with a high mortality rate. Patients with PF commonly experience a chronic dry cough and progressive dyspnoea for years without effective mitigation. The pathogenesis of PF is believed to be associated with dysfunctional macrophage polarization, fibroblast proliferation, and the loss of epithelial cells. Thus, it is of great importance and necessity to explore the interactions among macrophages, fibroblasts, and alveolar epithelial cells in lung fibrosis, as well as in the pro-fibrotic microenvironment.

Myofibroblast

J Cell Sci 1 July ; 13 : jcs Now, myofibroblasts are not only recognized for their physiological role in tissue repair but also as cells that are key in promoting the development of fibrosis in all organs. In this Cell Science at a Glance and the accompanying poster, we provide an overview of the current understanding of central aspects of myofibroblast biology, such as their definition, activation from different precursors, the involved signaling pathways and most widely used models to study their function. Myofibroblasts will be placed into context with their extracellular matrix and with other cell types communicating in the fibrotic environment. Furthermore, the challenges and strategies to target myofibroblasts in anti-fibrotic therapies are summarized to emphasize their crucial role in disease progression. Myofibroblasts have crucial physiological roles in rapidly repairing injured tissues by laying down collagen scar, like in skin after trauma or heart after cardiac infarction. In addition, myofibroblasts are key effector cells in almost all organ fibrosis by persistently accumulating and contracting scar tissue beyond normal repair Hinz, a ; Horowitz and Thannickal,

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In addition to direct intercellular communication, myofibroblast transmission of force to fibrous ECM generates mechanical signals see poster. Single-cell analysis reveals fibroblast heterogeneity and myofibroblasts in systemic sclerosis-associated interstitial lung disease. Wound-healing studies in cornea and skin: parallels, differences and opportunities. Longitudinal scRNAseq studies and meta-analysis over multiple independent studies will be required to decide whether computed similarity clusters reveal distinct fibroblast classes or represent transition stages. Wynn, T. Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. J Dent Res. Interleukin promotes cardiac fibrosis and myocardial stiffening in heart failure with preserved ejection fraction. If this clutch can support the loading force exerted by the myosin II on the cell membrane receptors, the maturation of FAs lead to mechanotransduction depending on properties of the environment where the cell reside in Sheetz , Geiger et al. It therefore seems appropriate to now try to control the molecular mediators and epigenetic regulators involved in order to affect the pathogenesis of ocular fibrosis [ 59 ]. Seo and colleagues suggested that collagen fibre thickness held more pertinence over dictating myofibroblast differentiation independently from collagen quantity [ ]. Time- and compartment-resolved proteome profiling of the extracellular niche in lung injury and repair. ECM-remodeling and crosslinking factors, such as matrix metalloproteases, lysyl oxidases LOXs , LOX-like enzymes, tissue transglutaminases, advanced glycation end products and lysyl hydroxylases, can be targeted to change ECM mechanics Afratis et al. Emerging insights into the role of matrix metalloproteases as therapeutic targets in fibrosis. Several factors such as eye trauma [ 23 ], uveitis [ 21 ] or atopic dermatitis [ 24 , 25 ] have been identified as possible causes of opacification of the anterior lens capsule.

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BMP7-induced-Pten inhibits Akt and prevents renal fibrosis. Role of the nuclear membrane protein Emerin in front-rear polarity of the nucleus. At the same time, these efforts also highlight the possibility of using cellular environmental properties not only to gain in-depth understanding of the FMT process, but also to control and manipulate it. The accumulation of EDA—FN has been observed in multiple fibrotic disorders, including lung, liver, and skin [ , , , ]. The roles of these mechanotransducer proteins in stress relay, which is involved in myofibroblast differentiation, will become clearer with continued investigation. Lagares et al. The organization of myofibroblasts at the borders of tumors with the neovasculature helps in the stabilization of tumor induced neovasculature. The activation of Wnt signalling was implicated in the fibrogenesis of multiple organs [ 82 ]. These results were recapitulated in rabbit ear hypertrophic scar models, wherein ABT improved scar appearance and collagen arrangement [ 40 ]. Al-Alawi, M. These studies showed that myofibroblast activity could be mediated through regulated leukocyte—myofibroblast interactions and suggest that targeting certain leukocyte subpopulations may serve as anti-fibrotic strategies. Mechanical tension controls granulation tissue contractile activity and myofibroblast differentiation. In this review, we focus on the best described roles of myofibroblasts during wound healing and fibrosis. Halder G. A more physiological 3D environment can also be reproduced using gels, such as collagen I hydrogels to model pulmonary fibrotic tissues coupled to a fibrosis-on-chip model Sundarakrishnan et al.