Relevant bibliographies by topics / Myofibroblasrts

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Myofibroblasrts'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Myofibroblasrts"

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Poobalarahi, Felicitta, Catalin F. Baicu, and Amy D. Bradshaw. "Cardiac myofibroblasts differentiated in 3D culture exhibit distinct changes in collagen I production, processing, and matrix deposition." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (2006): H2924—H2932. http://dx.doi.org/10.1152/ajpheart.00153.2006.

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Myofibroblasts are a differentiated fibroblast cell type characterized by increased contractile capacity and elevated production of extracellular matrix (ECM) proteins. In the heart, myofibroblast expression is implicated in fibrosis associated with pressure-overload hypertrophy, among other pathologies. Although enhanced expression of ECM proteins by myofibroblasts is established, few studies have addressed the nature of the ECM deposited by myofibroblasts. To characterize ECM production and assembly by cardiac myofibroblasts, we developed a three-dimensional (3D) culture system using primary
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Lapthorn, Alice, Marcus Ilg, Justine Sullivan, Peter Dziewulski, and Selim Cellek. "P03 Hydroxypyridone antifungals induce myofibroblast apoptosis in an in vitro model of hypertrophic scars." British Journal of Dermatology 189, no. 1 (2023): e15-e15. http://dx.doi.org/10.1093/bjd/ljad174.025.

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Abstract Despite being the most common complication following burn injury, there are no medications to prevent the formation of hypertrophic scars. Myofibroblasts are key cells involved in scar formation, responsible for producing excessive amounts of extracellular matrix and have been shown to be resistant to apoptosis. We have previously shown that hydroxypyridone antifungals can inhibit the transformation of fibroblasts to myofibroblasts, and exhibit other antifibrotic effects. This study aimed to investigate the effect of these drugs on established myofibroblasts. Primary human dermal fibr
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Wipff, Pierre-Jean, Daniel B. Rifkin, Jean-Jacques Meister та Boris Hinz. "Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix". Journal of Cell Biology 179, № 6 (2007): 1311–23. http://dx.doi.org/10.1083/jcb.200704042.

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The conjunctive presence of mechanical stress and active transforming growth factor β1 (TGF-β1) is essential to convert fibroblasts into contractile myofibroblasts, which cause tissue contractures in fibrotic diseases. Using cultured myofibroblasts and conditions that permit tension modulation on the extracellular matrix (ECM), we establish that myofibroblast contraction functions as a mechanism to directly activate TGF-β1 from self-generated stores in the ECM. Contraction of myofibroblasts and myofibroblast cytoskeletons prepared with Triton X-100 releases active TGF-β1 from the ECM. This pro
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Haas, MaryEllen R., Darlene V. Nguyen, and Brett A. Shook. "Recovery of Altered Diabetic Myofibroblast Heterogeneity and Gene Expression Are Associated with CD301b+ Macrophages." Biomedicines 9, no. 12 (2021): 1752. http://dx.doi.org/10.3390/biomedicines9121752.

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Diabetic wound healing is associated with impaired function and reduced numbers of myofibroblasts, a heterogeneous cell population with varying capacities to promote repair. To determine how diabetes alters myofibroblast composition, we performed flow cytometry and spatial tissue analysis of myofibroblast subsets throughout the healing process in diabetic (db/db) and control (db/+) mouse skin. We observed reduced numbers of profibrotic SCA1+; CD34+; CD26+ myofibroblasts in diabetic wounds five days after injury, with decreased expression of fibrosis-associated genes compared to myofibroblasts
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Mewhort, Holly E. M., Brodie D. Lipon, Daniyil A. Svystonyuk та ін. "Monocytes increase human cardiac myofibroblast-mediated extracellular matrix remodeling through TGF-β1". American Journal of Physiology-Heart and Circulatory Physiology 310, № 6 (2016): H716—H724. http://dx.doi.org/10.1152/ajpheart.00309.2015.

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Following myocardial infarction (MI), cardiac myofibroblasts remodel the extracellular matrix (ECM), preventing mechanical complications. However, prolonged myofibroblast activity leads to dysregulation of the ECM, maladaptive remodeling, fibrosis, and heart failure (HF). Chronic inflammation is believed to drive persistent myofibroblast activity; however, the mechanisms are unclear. We assessed the influence of peripheral blood monocytes on human cardiac myofibroblast activity in a three-dimensional (3D) ECM microenvironment. Human cardiac myofibroblasts isolated from surgical biopsies of the
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Rice, Nancy A., and Leslie A. Leinwand. "Skeletal myosin heavy chain function in cultured lung myofibroblasts." Journal of Cell Biology 163, no. 1 (2003): 119–29. http://dx.doi.org/10.1083/jcb.200303194.

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Myofibroblasts are unique contractile cells with both muscle and nonmuscle properties. Typically myofibroblasts are identified by the expression of α smooth muscle actin (ASMA); however some myofibroblasts also express sarcomeric proteins. In this study, we show that pulmonary myofibroblasts express three of the eight known sarcomeric myosin heavy chains (MyHCs) (IIa, IId, and embryonic) and that skeletal muscle myosin enzymatic activity is required for pulmonary myofibroblast contractility. Furthermore, inhibition of skeletal myosin activity and myofibroblast contraction results in a decrease
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Baum, Jennifer R., Biao Long, Candido Cabo, and Heather S. Duffy. "Myofibroblasts cause heterogeneous Cx43 reduction and are unlikely to be coupled to myocytes in the healing canine infarct." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (2012): H790—H800. http://dx.doi.org/10.1152/ajpheart.00498.2011.

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Following myocardial infarction (MI) inflammatory responses transform cardiac fibroblasts to myofibroblasts, which in vitro studies show form heterocellular gap junctions with cardiac myocytes via Connexin43 (Cx43). The ability to form heterocellular junctions in the intact heart and the impact of these junctions on propagation is unclear. We used a canine model of MI and characterized the distribution and quantity of myofibroblasts in surviving epicardial cells [epicardial border zone (EBZ)]. We found a significant increase in myofibroblasts within the EBZ and no gap junction plaques between
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Sánchez, Jorge, Beatriz Trenor, Javier Saiz, Olaf Dössel, and Axel Loewe. "Fibrotic Remodeling during Persistent Atrial Fibrillation: In Silico Investigation of the Role of Calcium for Human Atrial Myofibroblast Electrophysiology." Cells 10, no. 11 (2021): 2852. http://dx.doi.org/10.3390/cells10112852.

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During atrial fibrillation, cardiac tissue undergoes different remodeling processes at different scales from the molecular level to the tissue level. One central player that contributes to both electrical and structural remodeling is the myofibroblast. Based on recent experimental evidence on myofibroblasts’ ability to contract, we extended a biophysical myofibroblast model with Ca2+ handling components and studied the effect on cellular and tissue electrophysiology. Using genetic algorithms, we fitted the myofibroblast model parameters to the existing in vitro data. In silico experiments show
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Lodyga, Monika, Elizabeth Cambridge, Henna M. Karvonen та ін. "Cadherin-11–mediated adhesion of macrophages to myofibroblasts establishes a profibrotic niche of active TGF-β". Science Signaling 12, № 564 (2019): eaao3469. http://dx.doi.org/10.1126/scisignal.aao3469.

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Macrophages contribute to the activation of fibroblastic cells into myofibroblasts, which secrete collagen and contract the collagen matrix to acutely repair injured tissue. Persistent myofibroblast activation leads to the accumulation of fibrotic scar tissue that impairs organ function. We investigated the key processes that turn acute beneficial repair into destructive progressive fibrosis. We showed that homotypic cadherin-11 interactions promoted the specific binding of macrophages to and persistent activation of profibrotic myofibroblasts. Cadherin-11 was highly abundant at contacts betwe
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Honey, Nafzia, and Niroshini Rajaram. "The Dynamic Role Of Myofibroblasts In Oral Tissue Homeostasis And Disease." International Journal of Histopathological Interpretation 13, no. 1 (2024): 11–16. http://dx.doi.org/10.56501/intjhistopatholinterpret.v13i1.1047.

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Myofibroblasts are specialized cells that play a crucial role in maintaining the structural integrity and function of oral tissues. These cells exhibit a unique phenotype marked by the expression of alpha-smooth muscle actin (α-SMA), and possess the ability to contract and produce extracellular matrix components. In healthy oral tissues, myofibroblasts contribute to tissue homeostasis by mediating wound healing, tissue remodeling, and matrix turnover. However, the dysregulation of myofibroblast function can lead to pathological conditions such as fibrosis, scarring, and oral cancer. This revie
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Dissertations / Theses on the topic "Myofibroblasrts"

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Lecru, Lola. "Les récepteurs cannabinoïdes : une nouvelle cible thérapeutique de la fibrogenèse rénale." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T088.

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L’insuffisance rénale chronique et la dysfonction chronique de l’allogreffe (DCA) sont associées à la fibrogenèse rénale, qui représente un enjeu majeur en santé publique et nécessite l’exploration de nouvelles cibles thérapeutiques. Dans ce contexte, nous avons étudié l’expression des gènes modulés au cours d’un modèle reconnu de fibrogenèse chez la souris (le modèle d’obstruction urétérale unilatéral, ou OUU). L'expression du gène codant pour le récepteur cannabinoïde apparait sept fois augmentée dans les reins pathologiques comparée à leurs contrôles internes. L’expression du récepteur est
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Le, Hecho Sara. "Les myofibroblastes portaux : fonction angiogénique et implication dans la progression de la fibrose hépatique." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066252/document.

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Dans les maladies chroniques du foie, l’angiogenèse et la fibrose sont étroitement liées. Nosprécédents travaux ont permis de montrer que les myofibroblastes portaux (MFP)contribuaient de façon importante à la fibrogenèse hépatique. L’objectif de ma thèse était dedéterminer si les MFP pouvaient aussi contribuer à l’angiogenèse hépatique. Nous avonsidentifié un nouveau marqueur spécifique des MFP, le collagène XV, grâce auquel nousavons pu mettre en évidence une prolifération des MFP dans des stades avancés de fibrose, àla fois dans des modèles animaux et chez les patients atteints d’hépatopath
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Sagnol, Sébastien. "Rôle du facteur de transcription de ciliogenèse RFX3 dans le développement pulmonaire chez la souris." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10329.

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La protéine RFX3 appartient à une famille de facteurs de transcription RFX (Regulatory Factor X) très conservée au cours de l'évolution. Avec plusieurs autres membres de cette famille, RFX3 est impliquée dans la régulation de l'expression de gènes nécessaires pour l'assemblage et la fonction des cils. L’objectif de mon travail de thèse a été de comprendre le rôle du facteur de transcription RFX3 au cours du développement du poumon de la souris. RFX3 est exprimée dès le début du développement pulmonaire dans les cellules du mésenchyme et de l'épithélium, de manière corrélée à la présence de cil
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Le, Guilcher Camille. "Rôle du récepteur purinergique P2X4 dans l'activation des myofibroblastes au cours de la fibrogenèse hépatique." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS570.

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La fibrose hépatique, résultante commune de toutes les hépatopathies chroniques, est caractérisée par une accumulation excessive de composants matriciels produits par les myofibroblastes hépatiques (MFH) consécutive à une inflammation prolongée. Sans traitement, elle est associée à une morbidité et une mortalité élevées. L'adénosine triphosphate (ATP) extracellulaire et ses récepteurs constituent un puissant réseau de signalisation dans le processus cicatriciel. Bien que le récepteur purinergique P2X4 (P2X4R) soit fortement exprimé dans le foie, ses fonctions au cours de la fibrose hépatique n
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Badid, Chérif. "Myofibroblastes : cellules cibles dans la fibrogenèse rénale." Lyon 1, 2000. http://www.theses.fr/2000LYO1T163.

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Kalouche, Georges. "Effets des récepteurs des prostaglandines EP2 et FP sur les altérations du trabeculum : implication dans la pathologie glaucomateuse." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066294.

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Le glaucome est défini par une dégénérescence du nerf optique dont le principal facteur de risque est l’hypertension oculaire due à des altérations du tissu trabéculaire. Les traitements incluent des agonistes du récepteur FP, les agonistes du récepteur EP2 pouvant également avoir des effets bénéfiques.Au cours de cette thèse, un modèle de cellules trabéculaires primaires humaines a été défini et les effets du latanoprost, un agoniste FP, et du butaprost, un agoniste EP2, ont été étudiés, d'une part, sur la survie des cellules trabéculaires, et d’autre part, sur la transition myofibroblastique
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Corin, Karolina A. (Karolina Ann) 1981. "Inhibition of myofibroblast contraction." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/32381.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2005.<br>Includes bibliographical references (p. 46-49).<br>Although current medical procedures cannot restore complete function of a transected nerve, inserting both of its ends in a tube helps it regenerate. The regenerate is inferior to the uninjured nerve: it has a smaller diameter and poorer electrical conduction. Layers of contractile cells known as myofibroblasts have been observed around regenerated nerve portions. An inverse relationship between the layer thickness and the quality of the regenerate
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Suleman, Verjee Liaquat. "Myofibroblasts and the pathogenesis of Dupuytren's disease." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6119.

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Dupuytren’s disease is defined in Green’s Operative Hand Surgery as a condition of the hand characterised by the development of new tissue in the form of nodules and cords. Hand function can be significantly impaired and whilst the mainstay of treatment is surgery, recurrence has been reported in approximately 40-50% of patients. Myofibroblasts are central to the pathogenesis of Dupuytren’s disease although what regulates the myofibroblast phenotype during Dupuytren’s disease remains unclear. This thesis set out to test the hypothesis that the myofibroblast phenotype in Dupuytren’s disease is
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Kasabova, Mariana. "Rôle des cathepsines à cystéine et leurs inhibiteurs naturels, les cystatines lors de la fibrose pulmonaire." Thesis, Tours, 2013. http://www.theses.fr/2013TOUR4052.

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Lors de la fibrose pulmonaire idiopathique (FPI), la différenciation fibroblastique s’accompagne d’une accumulation excessive des composants de la matrice extracellulaire ainsi qu’à un dérèglement de la balance protéases / antiprotéases. Nous avons étudié le rôle des cathepsines à cystéine dans la myofibrogenèse et leur contribution potentielle à la physiopathologie de la fibrose pulmonaire chez l’Homme. Pour cela, le profil d’expression des cathepsines ainsi que de leurs inhibiteurs naturels a été évalué dans un modèle cellulaire expérimental, puis dans des myofibroblastes primaires et enfin
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Vernon, Madeleine Anne. "Myofibroblast loss during renal remodelling." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/9939.

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Renal fibrosis, the final endpoint of renal disease of any cause, is characterised by myofibroblast deposition of extracellular matrix (ECM) and commonly studied using the unilateral ureteric obstruction (UUO) model. Macrophages are multifunctional cells and involved in renal injury, repair and scarring. Work in other organs has shown that fibrosis is not necessarily irreversible and we established and characterised the murine model of reversible unilateral ureteric obstruction (R-UUO) to investigate the potential reversibility of fibrosis and the underlying mechanism with a particular focus u
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Books on the topic "Myofibroblasrts"

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Hinz, Boris, and David Lagares, eds. Myofibroblasts. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1382-5.

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Chaponnier, Christine, Alexis Desmoulière, and Giulio Gabbiani. Tissue Repair, Contraction and the Myofibroblast. Springer US, 2006. http://dx.doi.org/10.1007/0-387-33650-8.

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L, Granzier Henk, and Pollack Gerald H, eds. Elastic filaments of the cell. Kluwer Academic/Plenum Publishers, 2000.

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Kanta, Jiri, Alena Mrkvicová, and Ralf Weiskirchen, eds. Liver Myofibroblasts. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-989-1.

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Hinz, Boris, and David Lagares. Myofibroblasts: Methods and Protocols. Springer, 2021.

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Hinz, Boris, and David Lagares. Myofibroblasts: Methods and Protocols. Springer, 2021.

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Martinez, Analise. Myofibroblasts: Origin, Function and Role in Disease. Nova Science Publishers, Incorporated, 2016.

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Wound Healing, Fibrosis, and the Myofibroblast. Elsevier, 2022. http://dx.doi.org/10.1016/c2020-0-03642-x.

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Chaponnier, Christine, Christine Chaponnier, Alexis Desmoulière, and Giulio Gabbiani. Tissue Repair, Contraction and the Myofibroblast. Springer, 2011.

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Bunker, Tim D. Frozen shoulder. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.004005.

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♦ Frozen shoulder is caused by a contracture of the capsule♦ Counterintuitively not all patients recover completely♦ At arthroscopy spectacular angiogenesis is seen♦ Pathology shows bands and nodules of type III collagen populated by fibroblasts and myofibroblasts♦ Arthroscopic capsular release has improved the management of this condition.
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Book chapters on the topic "Myofibroblasrts"

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Darby, Ian A., and Alexis Desmoulière. "Scar Formation: Cellular Mechanisms." In Textbook on Scar Management. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_3.

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AbstractFibroblasts are key players in the maintenance of skin homeostasis and in orchestrating physiological tissue repair. Fibroblasts secrete and are embedded in a sophisticated extracellular matrix, and a complex and interactive dialogue exists between fibroblasts and their microenvironment. In addition to the secretion of the extracellular matrix, fibroblasts and myofibroblasts secrete extracellular matrix remodeling enzymes, matrix metalloproteinases and their inhibitors, and tissue inhibitors of metalloproteinases and are thus able to remodel the extracellular matrix. Myofibroblasts and
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Gabbiani, Giulio. "50 Years of Myofibroblasts: How the Myofibroblast Concept Evolved." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1382-5_1.

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Akers, lan A., Robin J. McAnulty, and Geoffrey J. Laurent. "Fibroblasts and myofibroblasts." In Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_6.

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Izumi, Motoyoshi, and Koichi Suda. "Pancreatic Ductal Myofibroblasts." In Pancreas - Pathological Practice and Research. KARGER, 2007. http://dx.doi.org/10.1159/000100401.

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Schürch, W. "The Myofibroblast in Neoplasia." In Current Topics in Pathology. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58456-5_14.

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Phan, Sem H. "Mechanisms of Myofibroblast Differentiation." In Dupuytren’s Disease and Related Hyperproliferative Disorders. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-22697-7_8.

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McCulloch, Christopher A. "Myofibroblast Adhesome Analysis by." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1382-5_5.

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Zimina, Elena, and Boris Hinz. "The Stressful Life of Cardiac Myofibroblasts." In Cardiac Fibrosis and Heart Failure: Cause or Effect? Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17437-2_5.

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Gabbiani, G. "CYTOSKELETAL AND CYTOCONTRACTILE FEATURES OF MYOFIBROBLASTS." In Proceedings of the Third Symposium, Lyon, France, June 26–28, 1985, edited by Jacques Bienvenu, J. A. Grimaud, and Philippe Laurent. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110860757-050.

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Gabbiani, Giulio. "Cytoskeletal and Cytocontractile Features of Myofibroblasts." In Interaction of Cells with Natural and Foreign Surfaces. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2229-0_4.

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Conference papers on the topic "Myofibroblasrts"

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Nathan, Adam C., Sheng-Lin Lee, J. Pablo Marquez, et al. "Active and Passive Responses of Myofibroblasts in Response to Mechanical Stretching in 3D Culture." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193101.

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The stretch response of myofibroblast cells cultured in a three-dimensional environment was simultaneously measured and observed using a tissue stretching apparatus mounted to a confocal microscope. Optical measurements were used to assess mechanical estimates of cell response obtained through combined mechanical testing and biochemical inhibition. Results show that activated myofibroblasts provide an effective resistance on the order of 100s of kPa. In specific mechanical environments, stretched myofibroblasts release the ECM.
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Kural, Mehmet H., and Kristen L. Billiar. "Effect of Boundary Stiffness on Contractility Profile of Valvular Interstitial Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14100.

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Heart valve disease leads to approximately 300,000 heart valve replacement surgeries each year worldwide. Valvular interstitial cells (VICs) are believed to play a vital role in the repair of heart valves and also most disease processes. VICs synthesize, remodel, and repair the ECM; however, when VICs excessively differentiate to the highly contractile and synthetic myofibroblast phenotype, valvular fibrosis may ensue. Elevated mechanical stress triggers the differentiation of VICs into myofibroblasts. Transforming growth factor beta-1 (TGF-β1) is also critical for the formation of thicker str
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Fee, Timothy J., Yong Zhou, Lauren E. Marshall, and Joel L. Berry. "The Strain Response of Lung Myofibroblasts Cultured on Electrospun Polycaprolactone Nanofibers." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14262.

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Idiopathic Pulmonary Fibrosis is a devastating condition characterized by excessive localized production of collagen in the lungs. Over 131,000 people are living with IPF in America (1, 2). There is currently no known treatment or cure for the disease. It has recently been shown that IPF myofibroblasts are sensitive to the stiffness of their substrate. Specifically, alpha Smooth Muscle Actin (alpha-SMA), a known indicator of IPF activity, was differentially produced on soft vs. stiff substrates (3). This suggests a mechanotransduction pathway within the IPF myofibroblasts.
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Galie, Peter A., та Jan P. Stegemann. "Cyclic Strain and Interstitial Flow Modulate Cardiac Fibroblast Phenotype Through Angiotensin II and TGF-β Pathways". У ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53924.

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A fibrotic scar in the myocardium is characterized by excessive extracellular matrix deposition, loss of functioning cardiomyocytes, and the transition of healthy cardiac fibroblasts to a myofibroblast phenotype. Previous research has suggested that the myofibroblast transition is mediated by mechanical stimuli including cyclic strain [1–2] and interstitial fluid flow [3–5].
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Sewell-Loftin, M. K., and W. David Merryman. "The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53604.

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Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following t
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Zhao, Ruogang, Lina Lin, and Craig A. Simmons. "The Effects of Cell Contraction and Loss of Adhesion on the Apoptosis of Valve Interstitial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19249.

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Dystrophic calcification in sclerotic aortic valves is associated with apoptosis of myofibroblasts that differentiate from valve interstitial cells (VICs). The factors that regulate apoptosis in sclerotic valves are not known, but may include mechanical stimuli, as is the case in other fibrotic tissues. In support of this hypothesis, we have observed that VICs on stiff collagen matrices that simulate fibrotic tissue differentiate to myofibroblasts and form calcified aggregates that contain apoptotic cells [1]. However, the mechanisms by which cell aggregation leads to VIC apoptosis are unknown
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Kalgudde Gopal, S., R. Dai, A. M. Stefanska, et al. "Wound Infiltrating Adipocytes Are Not Myofibroblasts." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2487.

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Sanchez, Cecilia G., Fuselier Taylor, Marguerite Changala, Fayong Luo, and Joseph A. Lasky. "Nelfinavir Inhibits Myofibroblasts Differentiation And Induces Autophagic Degradation Of Type I Collagen In Human Lung Myofibroblasts." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3505.

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Merryman, W. David, and Joshua D. Hutcheson. "Controlling the Mechanical Myofibroblast via SRC: A Potential Drug Discovery Platform." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19187.

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Abstract:
Connective tissue makes up a large portion of our bodies, with collagen constituting ∼30% of the protein of connective tissue. Any tissue that undergoes fibrosis, either due to a genetic mutation or with age or use, typically falls into the ubiquitous category of ‘connective tissue fibrosis’. There are multiple potential contributors to connective tissue fibrosis; however, two dominate the literature — mechanical stress/strain and cytokines. Both stimuli lead to activation of fibroblast cells to a myofibroblast phenotype, the cellular hallmark of fibrotic disease. The myofibroblast phenotype i
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Rafalskaya, A. V. "A PERSPECTIVE APPROACH TO THE TREATMENT OF DISEASES CAUSED BY TISSUE FIBROSIS USING THE SECRETOME OF MESENCHYMAL STEM CELLS." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute, 2021. http://dx.doi.org/10.46646/sakh-2021-1-321-324.

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In this article the problems of pathological differentiation of myofibroblasts, leading to idiopathic pulmonary fibrosis are highlighted. Among the modern methods of therapy, special attention is paid to the cellular approach ,in particular, the use of mesenchymal stem cells. A method of influencing the process of scarring of lung tissue using the secretome of mesenchymal stem cells with properties for medical and therapeutic use was proposed.
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