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Artigos de revistas sobre o tema "Extracellular matrix Physiology"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 28 de janeiro de 2023

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1

Roman, Jesse, Andrew H. Limper, and John A. McDonald. "Lung Extracellular Matrix: Physiology and Pathophysiology." Hospital Practice 25, no. 11 (November 15, 1990): 125–40. http://dx.doi.org/10.1080/21548331.1990.11704038.

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2

Bloksgaard, Maria, Merry Lindsey, and Luis A. Martinez-Lemus. "Extracellular matrix in cardiovascular pathophysiology." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (December 1, 2018): H1687—H1690. http://dx.doi.org/10.1152/ajpheart.00631.2018.

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The extracellular matrix (ECM) actively participates in diverse aspects of cardiovascular development and physiology as well as during disease development and progression. ECM roles are determined by its physical and mechanical properties and by its capacity to both release bioactive signals and activate cell signaling pathways. The ECM serves as a storage depot for a wide variety of molecules released in response to injury or with aging. Indeed, there is a plethora of examples describing how cells react to or modify ECM stiffness, how cells initiate intracellular signaling pathways, and how c

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3

Wijsman, Pieta C., Lisa H. van Smoorenburg, Daniël M. de Bruin, Jouke T. Annema, Huib AM Kerstjens, Onno M. Mets, Maarten van den Berge, Peter I. Bonta, and Janette K. Burgess. "Imaging the pulmonary extracellular matrix." Current Opinion in Physiology 22 (August 2021): 100444. http://dx.doi.org/10.1016/j.cophys.2021.05.007.

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4

Rienks, Marieke, Anna-Pia Papageorgiou, Nikolaos G. Frangogiannis, and Stephane Heymans. "Myocardial Extracellular Matrix." Circulation Research 114, no. 5 (February 28, 2014): 872–88. http://dx.doi.org/10.1161/circresaha.114.302533.

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5

Davis, George E., and Donald R. Senger. "Endothelial Extracellular Matrix." Circulation Research 97, no. 11 (November 25, 2005): 1093–107. http://dx.doi.org/10.1161/01.res.0000191547.64391.e3.

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6

Tayebjee, Muzahir H., Robert J. MacFadyen, and Gregory YH Lip. "Extracellular matrix biology." Journal of Hypertension 21, no. 12 (December 2003): 2211–18. http://dx.doi.org/10.1097/00004872-200312000-00002.

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7

Ramirez, Francesco, Lynn Y. Sakai, Harry C. Dietz, and Daniel B. Rifkin. "Fibrillin microfibrils: multipurpose extracellular networks in organismal physiology." Physiological Genomics 19, no. 2 (October 4, 2004): 151–54. http://dx.doi.org/10.1152/physiolgenomics.00092.2004.

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Organismal physiology depends significantly on the proper assembly of extracellular matrix (ECM) macroaggregates that impart structural integrity to the connective tissue. Recent genetic studies in mice have unraveled unsuspected new functions of architectural matrix components in regulating signaling events that modulate patterning, morphogenesis, and growth of several organ systems. As a result, a new paradigm has emerged whereby tissue-specific organization of the ECM dictates not only the physical properties of the connective tissue, but also the ability of the matrix to direct a broad spe

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8

Vogel, Viola. "Unraveling the Mechanobiology of Extracellular Matrix." Annual Review of Physiology 80, no. 1 (February 10, 2018): 353–87. http://dx.doi.org/10.1146/annurev-physiol-021317-121312.

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9

Brown, Lindsay. "Cardiac extracellular matrix: a dynamic entity." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H973—H974. http://dx.doi.org/10.1152/ajpheart.00443.2005.

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10

Ma, Zihan, Chenfeng Mao, Yiting Jia, Yi Fu, and Wei Kong. "Extracellular matrix dynamics in vascular remodeling." American Journal of Physiology-Cell Physiology 319, no. 3 (September 1, 2020): C481—C499. http://dx.doi.org/10.1152/ajpcell.00147.2020.

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Vascular remodeling is the adaptive response to various physiological and pathophysiological alterations that are closely related to aging and vascular diseases. Understanding the mechanistic regulation of vascular remodeling may be favorable for discovering potential therapeutic targets and strategies. The extracellular matrix (ECM), including matrix proteins and their degradative metalloproteases, serves as the main component of the microenvironment and exhibits dynamic changes during vascular remodeling. This process involves mainly the altered composition of matrix proteins, metalloproteas

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11

Gerecht, Sharon. "ANGIOGENESIS BIOMIMETIC: EXTRACELLULAR MATRIX AND OXYGEN." Free Radical Biology and Medicine 65 (November 2013): S13. http://dx.doi.org/10.1016/j.freeradbiomed.2013.10.412.

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12

Tyagi, Suresh C. "Physiology and homeostasis of extracellular matrix: cardiovascular adaptation and remodeling." Pathophysiology 7, no. 3 (September 2000): 177–82. http://dx.doi.org/10.1016/s0928-4680(00)00046-8.

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13

Dunsmore, S. E., and D. E. Rannels. "Extracellular matrix biology in the lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L3—L27. http://dx.doi.org/10.1152/ajplung.1996.270.1.l3.

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The lung and other organs are comprised of both cellular and extracellular compartments. Interaction of these components modulates physiological function at the organ, cellular, and subcellular levels. Extracellular components in the gas-exchange region of the lung include both noncellular interstitium and basement membranes. Connective tissue elements of the interstitium in part determine ventilatory function by contributions to tissue compliance and to resistance of the diffusion barrier. The basement membrane underlies cells of both the alveolar epithelium and the capillary endothelium; bas

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14

Luo, Xia, Lingyan Deng, Laxmi Pangeni Lamsal, Wenjuan Xu, Cheng Xiang, and Liming Cheng. "AMP-Activated Protein Kinase Alleviates Extracellular Matrix Accumulation in High Glucose-Induced Renal Fibroblasts through mTOR Signaling Pathway." Cellular Physiology and Biochemistry 35, no. 1 (2015): 191–200. http://dx.doi.org/10.1159/000369687.

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Background/Aims: Extracellular matrix accumulation contributes significantly to the pathogenesis of diabetic nephropathy. Although AMP-activated protein kinase (AMPK) has been found to inhibit extracellular matrix synthesis by experiments in vivo and vitro, its role in alleviating the deposition of extracellular matrix in renal interstitial fibroblasts has not been well defined. Methods: Currently, we conducted this study to investigate the effects of AMPK on high glucose-induced extracellular matrix synthesis and involved intracellular signaling pathway by using western blot in the kidney fib

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15

Stauber, W. T., P. M. Clarkson, V. K. Fritz, and W. J. Evans. "Extracellular matrix disruption and pain after eccentric muscle action." Journal of Applied Physiology 69, no. 3 (September 1, 1990): 868–74. http://dx.doi.org/10.1152/jappl.1990.69.3.868.

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Pain, stiffness, and indicators of muscle damage occur at different times after eccentric muscle action. After a single bout of maximal resisted lengthening of the elbow flexors, elbow position, pain perception, and indicators of cellular damage were measured. Immediately postexercise, a significant decrease in resting muscle length was observed that continued to 48 h. At this time, an increase in perceived muscle soreness was noted (P less than 0.05), and a biopsy of the biceps brachii revealed mast cell degranulation, separations of the extracellular matrix from myofibers, and increased plas

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16

Arriazu, Elena, Marina Ruiz de Galarreta, Francisco Javier Cubero, Marta Varela-Rey, María Pilar Pérez de Obanos, Tung Ming Leung, Aritz Lopategi, Aitor Benedicto, Ioana Abraham-Enachescu, and Natalia Nieto. "Extracellular Matrix and Liver Disease." Antioxidants & Redox Signaling 21, no. 7 (September 2014): 1078–97. http://dx.doi.org/10.1089/ars.2013.5697.

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17

Arroyo, A. G., and M. L. Iruela-Arispe. "Extracellular matrix, inflammation, and the angiogenic response." Cardiovascular Research 86, no. 2 (February 12, 2010): 226–35. http://dx.doi.org/10.1093/cvr/cvq049.

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18

Abonnenc, Mélanie, Adam A. Nabeebaccus, Ursula Mayr, Javier Barallobre-Barreiro, Xuebin Dong, Friederike Cuello, Sumon Sur, et al. "Extracellular Matrix Secretion by Cardiac Fibroblasts." Circulation Research 113, no. 10 (October 25, 2013): 1138–47. http://dx.doi.org/10.1161/circresaha.113.302400.

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19

Siefert, Suzanne A., and Rajabrata Sarkar. "Matrix metalloproteinases in vascular physiology and disease." Vascular 20, no. 4 (August 2012): 210–16. http://dx.doi.org/10.1258/vasc.2011.201202.

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Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that primarily degrade components of the extracellular matrix (ECM). Remodeling of the ECM by MMPs is important in both physiological and pathological processes, including organ generation/regeneration, angiogenesis, wound healing, inflammation and tumor growth. In the vasculature, MMPs play a role in beneficial processes such as angiogenesis, collateral artery formation and thrombus resolution. However, MMP expression is also implicated in the pathogenesis of vascular diseases such as atherosclerosis, aortic aneury

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20

Tran, Thai, and Andrew J. Halayko. "Extracellular matrix and airway smooth muscle interactions: a target for modulating airway wall remodelling and hyperresponsiveness?This article is one of a selection of papers published in the Special Issue on Recent Advances in Asthma Research." Canadian Journal of Physiology and Pharmacology 85, no. 7 (July 2007): 666–71. http://dx.doi.org/10.1139/y07-050.

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The airway smooth muscle from asthmatic airways produces increased amounts and an altered composition of extracellular matrix proteins. The extracellular matrix can in turn influence the phenotype and function of airway smooth muscle cells, affecting the biochemical, geometric, and mechanical properties of the airway wall. This review provides a brief overview of the current understanding of the biology associated with airway smooth muscle interactions with the extracellular matrix. We present future directions needed for the study of cellular and molecular mechanisms that determine the outcom

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21

Forget, Marie-Annick, Richard R. Desrosiers, and Richard Béliveau. "Physiological roles of matrix metalloproteinases: implications for tumor growth and metastasis." Canadian Journal of Physiology and Pharmacology 77, no. 7 (August 1, 1999): 465–80. http://dx.doi.org/10.1139/y99-055.

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Physiological processes involving remodelling of the extracellular matrix, such as wound healing, embryogenesis, angiogenesis, and the female reproductive cycle, require the activity of matrix metalloproteinases (MMPs). This group of proteases degrades basal membranes and connective tissues and plays an essential role in the homeostasis of the extracellular matrix. An imbalance in the expression or activity of MMPs can have important consequences in diseases such as multiple sclerosis, Alzheimer's disease, or the development of cancers. Because of the pathophysiological importance of MMPs, the

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22

Graham, H. K., M. Horn, and A. W. Trafford. "Extracellular matrix profiles in the progression to heart failure." Acta Physiologica 194, no. 1 (September 2008): 3–21. http://dx.doi.org/10.1111/j.1748-1716.2008.01881.x.

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23

Rodgers, Raymond. "Extracellular Matrix in the Ovary." Seminars in Reproductive Medicine 24, no. 4 (September 2006): 193–94. http://dx.doi.org/10.1055/s-2006-948548.

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24

Krishnan, Laxminarayanan, James B. Hoying, Hoa Nguyen, Helen Song, and Jeffrey A. Weiss. "Interaction of angiogenic microvessels with the extracellular matrix." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 6 (December 2007): H3650—H3658. http://dx.doi.org/10.1152/ajpheart.00772.2007.

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The extracellular matrix (ECM) plays a critical role in angiogenesis by providing biochemical and positional cues, as well as by mechanically influencing microvessel cell behavior. Considerable information is known concerning the biochemical cues relevant to angiogenesis, but less is known about the mechanical dynamics during active angiogenesis. The objective of this study was to characterize changes in the material properties of a simple angiogenic tissue before and during angiogenesis. During sprouting, there was an overall decrease in tissue stiffness followed by an increase during neovess

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25

Haas, Tara L. "Endothelial cell regulation of matrix metalloproteinases." Canadian Journal of Physiology and Pharmacology 83, no. 1 (January 1, 2005): 1–7. http://dx.doi.org/10.1139/y04-120.

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The process of sprouting angiogenesis requires that the endothelial cells degrade the basement membrane matrix and migrate into the interstitial matrix. Matrix metalloproteinases are enzymes capable of cleaving numerous extracellular matrix proteins. Increased production and activity of matrix metalloproteinases in any cell type is associated with a more migratory and invasive phenotype. This paper describes results of recent in-vitro studies of the regulation of transcription and activation of MMP-2 and MT1-MMP in endothelial cells, as well as studies that examined roles of matrix metalloprot

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26

Adams, Josephine Clare. "Molecular organisation of cell–matrix contacts: essential multiprotein assemblies in cell and tissue function." Expert Reviews in Molecular Medicine 4, no. 1 (February 11, 2002): 1–24. http://dx.doi.org/10.1017/s1462399402004039.

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The adhesion of cells to their surrounding extracellular matrix has vital roles in embryonic development, inflammatory responses, wound healing and adult tissue homeostasis. Cells attach to extracellular matrix by specific cell-surface receptors, of which the integrins and transmembrane proteoglycans are major representatives. The engagement of adhesion receptors triggers assembly of functional matrix contacts, in which bound matrix components, adhesion receptors and associated intracellular cytoskeletal and signalling molecules form large, localised multiprotein complexes. This review discuss

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27

McGowan, S. E., and R. J. Thompson. "Extracellular matrix proteoglycan degradation by human alveolar macrophages and neutrophils." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 400–409. http://dx.doi.org/10.1152/jappl.1989.66.1.400.

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Degradation and restructuring of the elastin fiber network of the lung is a pivotal process in the pathogenesis of emphysema. Alveolar macrophages and neutrophils are probably directly involved in elastin degradation, but they may also indirectly influence elastin structure and function by altering other extracellular matrix components such as proteoglycans. In this study the mechanisms of proteoglycan degradation by human alveolar macrophages and neutrophils have been explored. Macrophages appear to utilize plasminogen in solubilizing 35SO4-labeled proteoglycans in extracellular matrix produc

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28

Ito, Akira, Tomoki Aoyama, Hirotaka Iijima, Momoko Nagai, Shoki Yamaguchi, Junichi Tajino, Xiangkai Zhang, Haruhiko Akiyama, and Hiroshi Kuroki. "Optimum temperature for extracellular matrix production by articular chondrocytes." International Journal of Hyperthermia 30, no. 2 (February 5, 2014): 96–101. http://dx.doi.org/10.3109/02656736.2014.880857.

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29

de Haas, Hans J., Eloisa Arbustini, Valentin Fuster, Christopher M. Kramer, and Jagat Narula. "Molecular Imaging of the Cardiac Extracellular Matrix." Circulation Research 114, no. 5 (February 28, 2014): 903–15. http://dx.doi.org/10.1161/circresaha.113.302680.

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30

Andreeva, E. R., and D. K. Matveeva. "Multipotent Mesenchymal Stromal Cells and Extracellular Matrix: Regulation under Hypoxia." Human Physiology 44, no. 6 (November 2018): 696–705. http://dx.doi.org/10.1134/s0362119718060038.

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31

Kennett, Eleanor C., and Michael J. Davies. "Degradation of extracellular matrix by peroxynitrite/peroxynitrous acid." Free Radical Biology and Medicine 45, no. 5 (September 2008): 716–25. http://dx.doi.org/10.1016/j.freeradbiomed.2008.05.027.

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32

Borojevic, R. "Extracellular matrix: understanding the complexity." Brazilian Journal of Medical and Biological Research 32, no. 5 (May 1999): 497–99. http://dx.doi.org/10.1590/s0100-879x1999000500001.

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33

Stauber, W. T., V. K. Fritz, T. E. Burkovskaya, and E. I. Ilyina-Kakueva. "Effect of spaceflight on the extracellular matrix of skeletal muscle after a crush injury." Journal of Applied Physiology 73, no. 2 (August 1, 1992): S74—S81. http://dx.doi.org/10.1152/jappl.1992.73.2.s74.

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The organization and composition of the extracellular matrix were studied in the crush-injured gastrocnemius muscle of rats subjected to 0 G. After 14 days of flight on COSMOS 2044, the gastrocnemius muscle was removed and evaluated by histochemical and immunohistochemical techniques from the five injured flight rodents and various Earth-based treatment groups. In general, the repair process was similar in all injured muscle samples with regard to the organization of the extracellular matrix and myofibers. Small and large myofibers were present within an expanded extracellular matrix, indicati

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34

Syková, Eva, and Charles Nicholson. "Diffusion in Brain Extracellular Space." Physiological Reviews 88, no. 4 (October 2008): 1277–340. http://dx.doi.org/10.1152/physrev.00027.2007.

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Diffusion in the extracellular space (ECS) of the brain is constrained by the volume fraction and the tortuosity and a modified diffusion equation represents the transport behavior of many molecules in the brain. Deviations from the equation reveal loss of molecules across the blood-brain barrier, through cellular uptake, binding, or other mechanisms. Early diffusion measurements used radiolabeled sucrose and other tracers. Presently, the real-time iontophoresis (RTI) method is employed for small ions and the integrative optical imaging (IOI) method for fluorescent macromolecules, including de

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35

Bijian, Krikor, Tomoko Takano, Joan Papillon, Abdelkrim Khadir, and Andrey V. Cybulsky. "Extracellular matrix regulates glomerular epithelial cell survival and proliferation." American Journal of Physiology-Renal Physiology 286, no. 2 (February 2004): F255—F266. http://dx.doi.org/10.1152/ajprenal.00259.2003.

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Glomerular epithelial cell (GEC) injury and apoptosis may contribute to sclerosis in glomerulonephritis. The present study addresses signals that regulate survival of GEC in culture and in the acute puromycin aminonucleoside nephrosis (PAN) model of GEC injury in vivo. Compared with GEC on plastic substratum, adhesion to collagen increased activation of focal adhesion kinase (FAK), c-Src, and ERK and facilitated survival (prevented apoptosis). GEC on plastic exhibited increased caspase-8 and -9 activities, increased expression of the proapoptotic protein, Bax, and decreased the antiapoptotic p

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36

Bruggeman, L. A., E. A. Horigan, S. Horikoshi, P. E. Ray, and P. E. Klotman. "Thromboxane stimulates synthesis of extracellular matrix proteins in vitro." American Journal of Physiology-Renal Physiology 261, no. 3 (September 1, 1991): F488—F494. http://dx.doi.org/10.1152/ajprenal.1991.261.3.f488.

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The vasoconstrictor eicosanoid thromboxane plays an important role in the pathogenesis of several renal diseases. As an autacoid, its local release alters blood flow and induces platelet aggregation. We report a direct stimulatory effect of thromboxane on extracellular matrix protein production and gene expression in vitro. Treatment of two cell types, differentiated mouse teratocarcinoma cells (F9+) and human glomerular mesangial cells, with two different thromboxane analogues resulted in increased production of components of the extracellular matrix including fibronectin and the basement mem

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37

Savino, Wilson, and Joseli Lannes Vieira. "Is there a role for extracellular matrix in thymus physiology and pathology?" Memórias do Instituto Oswaldo Cruz 86, suppl 3 (1991): 91–97. http://dx.doi.org/10.1590/s0074-02761991000700013.

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Astudillo, Pablo. "Extracellular matrix stiffness and Wnt/β-catenin signaling in physiology and disease". Biochemical Society Transactions 48, № 3 (15 травня 2020): 1187–98. http://dx.doi.org/10.1042/bst20200026.

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The Wnt/β-catenin signaling pathway plays fundamental roles during development, stem cell differentiation, and homeostasis, and its abnormal activation can lead to diseases. In recent years, it has become clear that this pathway integrates signals not only from Wnt ligands but also from other proteins and signaling routes. For instance, Wnt/β-catenin signaling involves YAP and TAZ, which are transcription factors with crucial roles in mechanotransduction. On the other hand, Wnt/β-catenin signaling is also modulated by integrins. Therefore, mechanical signals might similarly modulate the Wnt/β-

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39

Schmidt, Roland, Andreas Bültmann, Martin Ungerer, Nader Joghetaei, Özgür Bülbül, Sven Thieme, Triantafyllos Chavakis, et al. "Extracellular Matrix Metalloproteinase Inducer Regulates Matrix Metalloproteinase Activity in Cardiovascular Cells." Circulation 113, no. 6 (February 14, 2006): 834–41. http://dx.doi.org/10.1161/circulationaha.105.568162.

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Zou, Huan, Rongdi Yuan, Qijun Zheng, Yan Huo, Min Lang, Shuxing Ji, Zheng Zheng, and Jian Ye. "Fluctuations in Intraocular Pressure Increase the Trabecular Meshwork Extracellular Matrix." Cellular Physiology and Biochemistry 33, no. 4 (2014): 1215–24. http://dx.doi.org/10.1159/000358691.

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Casals, Gregori, Guillermo Fernández-Varo, Pedro Melgar-Lesmes, Santi Marfà, Vedrana Reichenbach, Manuel Morales-Ruiz, and Wladimiro Jiménez. "Factors Involved in Extracellular Matrix Turnover in Human Derived Cardiomyocytes." Cellular Physiology and Biochemistry 32, no. 5 (2013): 1125–36. http://dx.doi.org/10.1159/000354513.

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McGee, Maria P., Michael J. Morykwas, James E. Jordan, Rui Wang, and Louis C. Argenta. "Local fluid transfer regulation in heart extracellular matrix." Journal of Physiology and Biochemistry 72, no. 2 (March 9, 2016): 255–68. http://dx.doi.org/10.1007/s13105-016-0473-9.

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Coffey, Elizabeth C., Mary Astumian, Sarah S. Alrowaished, Claire Schaffer, and Clarissa A. Henry. "Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix." Journal of Developmental Biology 9, no. 4 (November 23, 2021): 52. http://dx.doi.org/10.3390/jdb9040052.

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Muscle development and homeostasis are critical for normal muscle function. A key aspect of muscle physiology during development, growth, and homeostasis is modulation of protein turnover, the balance between synthesis and degradation of muscle proteins. Protein degradation depends upon lysosomal pH, generated and maintained by proton pumps. Sphingolipid transporter 1 (spns1), a highly conserved gene encoding a putative late endosome/lysosome carbohydrate/H+ symporter, plays a pivotal role in maintaining optimal lysosomal pH and spns1−/− mutants undergo premature senescence. However, the impac

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44

Yen, Chung-Jen, Cheng-Chung Fang, Yung-Ming Chen, Rong-Hwa Lin, Kwan-Dun Wu, Po-Huang Lee, and Tun-Jun Tsai. "Extracellular Matrix Proteins Modulate Human Peritoneal Mesothelial Cell Behavior." Nephron 75, no. 2 (1997): 188–95. http://dx.doi.org/10.1159/000189530.

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45

Freitas, Ana, Miguel Aroso, António Barros, Miriam Fernández, Eduardo Conde-Sousa, Marina Leite, Eva Daniela Carvalho, et al. "Characterization of the Striatal Extracellular Matrix in a Mouse Model of Parkinson’s Disease." Antioxidants 10, no. 7 (July 8, 2021): 1095. http://dx.doi.org/10.3390/antiox10071095.

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Parkinson’s disease’s etiology is unknown, although evidence suggests the involvement of oxidative modifications of intracellular components in disease pathobiology. Despite the known involvement of the extracellular matrix in physiology and disease, the influence of oxidative stress on the matrix has been neglected. The chemical modifications that might accumulate in matrix components due to their long half-live and the low amount of extracellular antioxidants could also contribute to the disease and explain ineffective cellular therapies. The enriched striatal extracellular matrix from a mou

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46

Penberthy, T. W., Y. Jiang, F. W. Luscinskas, and D. T. Graves. "MCP-1-stimulated monocytes preferentially utilize beta 2-integrins to migrate on laminin and fibronectin." American Journal of Physiology-Cell Physiology 269, no. 1 (July 1, 1995): C60—C68. http://dx.doi.org/10.1152/ajpcell.1995.269.1.c60.

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Recruitment of monocytes to inflammatory sites involves a series of sequential attachments and detachments to extracellular matrix proteins in response to a chemoattractant gradient. In this study we compared the migration of human peripheral blood monocytes on different extracellular matrix proteins in response to monocyte chemoattractant protein-1 (MCP-1) and N-formylmethionyl-leucyl-phenylalanine. Monocytes migrated more effectively on laminin compared with other extracellular matrix proteins. In contrast, this preference was not observed with neutrophils, suggesting that the monocytes and

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47

Fissell, William H., Christina L. Hofmann, Nicholas Ferrell, Lisa Schnell, Anna Dubnisheva, Andrew L. Zydney, Peter D. Yurchenco, and Shuvo Roy. "Solute partitioning and filtration by extracellular matrices." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F1092—F1100. http://dx.doi.org/10.1152/ajprenal.00162.2009.

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The physiology of glomerular filtration remains mechanistically obscure despite its importance in disease. The correspondence between proteinuria and foot process effacement suggests podocytes as the locus of the filtration barrier. If so, retained macromolecules ought to accumulate at the filtration barrier, an effect called concentration polarization. Literature data indicate macromolecule concentrations decrease from subendothelial to subepithelial glomerular basement membrane (GBM), as would be expected if the GBM were itself the filter. The objective of this study was to obtain insights i

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Aicher, Brittany O., Jackie Zhang, Selen C. Muratoglu, Rebeca Galisteo, Allison L. Arai, Vicki L. Gray, Brajesh K. Lal, Dudley K. Strickland, and Areck A. Ucuzian. "Moderate aerobic exercise prevents matrix degradation and death in a mouse model of aortic dissection and aneurysm." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 5 (May 1, 2021): H1786—H1801. http://dx.doi.org/10.1152/ajpheart.00229.2020.

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Moderate aerobic exercise was shown to significantly reduce mortality, extracellular matrix degradation, and thoracic aortic aneurysm and dissection formation associated with lysyl oxidase inhibition in a mouse model. Gene expression suggested a reversal of TGF-β, inflammation, and extracellular matrix remodeling pathway dysregulation, along with augmented elastogenesis with exercise.

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Irving-Rodgers, Helen, Jan Roger, Martin Luck, and Raymond Rodgers. "Extracellular Matrix of the Corpus Luteum." Seminars in Reproductive Medicine 24, no. 4 (September 2006): 242–50. http://dx.doi.org/10.1055/s-2006-948553.

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Berkholtz, Courtney, Lonnie Shea, and Teresa Woodruff. "Extracellular Matrix Functions in Follicle Maturation." Seminars in Reproductive Medicine 24, no. 4 (September 2006): 262–69. http://dx.doi.org/10.1055/s-2006-948555.

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