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Journal articles on the topic 'Mechanotransduction'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

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1

French, A. S. "Mechanotransduction." Annual Review of Physiology 54, no. 1 (October 1992): 135–52. http://dx.doi.org/10.1146/annurev.ph.54.030192.001031.

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2

Qin, Yi-Xian, and Minyi Hu. "Mechanotransduction in Musculoskeletal Tissue Regeneration: Effects of Fluid Flow, Loading, and Cellular-Molecular Pathways." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/863421.

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While mechanotransductive signal is proven essential for tissue regeneration, it is critical to determine specific cellular responses to such mechanical signals and the underlying mechanism. Dynamic fluid flow induced by mechanical loading has been shown to have the potential to regulate bone adaptation and mitigate bone loss. Mechanotransduction pathways are of great interests in elucidating how mechanical signals produce such observed effects, including reduced bone loss, increased bone formation, and osteogenic cell differentiation. The objective of this review is to develop a molecular understanding of the mechanotransduction processes in tissue regeneration, which may provide new insights into bone physiology. We discussed the potential for mechanical loading to induce dynamic bone fluid flow, regulation of bone adaptation, and optimization of stimulation parameters in various loading regimens. The potential for mechanical loading to regulate microcirculation is also discussed. Particularly, attention is allotted to the potential cellular and molecular pathways in response to loading, including osteocytes associated with Wnt signaling, elevation of marrow stem cells, and suppression of adipotic cells, as well as the roles of LRP5 and microRNA. These data and discussions highlight the complex yet highly coordinated process of mechanotransduction in bone tissue regeneration.
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3

Luis Alonso, José, and Wolfgang H. Goldmann. "Cellular mechanotransduction." AIMS Biophysics 3, no. 1 (2016): 50–62. http://dx.doi.org/10.3934/biophy.2016.1.50.

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4

Chalfie, Martin. "Neurosensory mechanotransduction." Nature Reviews Molecular Cell Biology 10, no. 1 (January 2009): 44–52. http://dx.doi.org/10.1038/nrm2595.

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5

Hansen, Caroline E., Yongzhi Qiu, Owen J. T. McCarty, and Wilbur A. Lam. "Platelet Mechanotransduction." Annual Review of Biomedical Engineering 20, no. 1 (June 4, 2018): 253–75. http://dx.doi.org/10.1146/annurev-bioeng-062117-121215.

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The vasculature is a dynamic environment in which blood platelets constantly survey the endothelium for sites of vessel damage. The formation of a mechanically coherent hemostatic plug to prevent blood loss relies on a coordinated series of ligand–receptor interactions governing the recruitment, activation, and aggregation of platelets. The physical biology of each step is distinct in that the recruitment of platelets depends on the mechanosensing of the platelet receptor glycoprotein Ib for the adhesive protein von Willebrand factor, whereas platelet activation and aggregation are responsive to the mechanical forces sensed at adhesive junctions between platelets and at the platelet–matrix interface. Herein we take a biophysical perspective to discuss the current understanding of platelet mechanotransduction as well as the measurement techniques used to quantify the physical biology of platelets in the context of thrombus formation under flow.
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6

Persat, Alexandre. "Bacterial mechanotransduction." Current Opinion in Microbiology 36 (April 2017): 1–6. http://dx.doi.org/10.1016/j.mib.2016.12.002.

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7

Leckband, Deborah. "Intercellular Mechanotransduction." Biophysical Journal 114, no. 3 (February 2018): 555a. http://dx.doi.org/10.1016/j.bpj.2017.11.3033.

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8

Stewart, Sarah, Alastair Darwood, Spyros Masouros, Claire Higgins, and Arul Ramasamy. "Mechanotransduction in osteogenesis." Bone & Joint Research 9, no. 1 (January 2020): 1–14. http://dx.doi.org/10.1302/2046-3758.91.bjr-2019-0043.r2.

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Bone is one of the most highly adaptive tissues in the body, possessing the capability to alter its morphology and function in response to stimuli in its surrounding environment. The ability of bone to sense and convert external mechanical stimuli into a biochemical response, which ultimately alters the phenotype and function of the cell, is described as mechanotransduction. This review aims to describe the fundamental physiology and biomechanisms that occur to induce osteogenic adaptation of a cell following application of a physical stimulus. Considerable developments have been made in recent years in our understanding of how cells orchestrate this complex interplay of processes, and have become the focus of research in osteogenesis. We will discuss current areas of preclinical and clinical research exploring the harnessing of mechanotransductive properties of cells and applying them therapeutically, both in the context of fracture healing and de novo bone formation in situations such as nonunion. Cite this article: Bone Joint Res 2019;9(1):1–14.
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9

Uray, Iván P., and Karen Uray. "Mechanotransduction at the Plasma Membrane-Cytoskeleton Interface." International Journal of Molecular Sciences 22, no. 21 (October 26, 2021): 11566. http://dx.doi.org/10.3390/ijms222111566.

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Mechanical cues are crucial for survival, adaptation, and normal homeostasis in virtually every cell type. The transduction of mechanical messages into intracellular biochemical messages is termed mechanotransduction. While significant advances in biochemical signaling have been made in the last few decades, the role of mechanotransduction in physiological and pathological processes has been largely overlooked until recently. In this review, the role of interactions between the cytoskeleton and cell-cell/cell-matrix adhesions in transducing mechanical signals is discussed. In addition, mechanosensors that reside in the cell membrane and the transduction of mechanical signals to the nucleus are discussed. Finally, we describe two examples in which mechanotransduction plays a significant role in normal physiology and disease development. The first example is the role of mechanotransduction in the proliferation and metastasis of cancerous cells. In this system, the role of mechanotransduction in cellular processes, including proliferation, differentiation, and motility, is described. In the second example, the role of mechanotransduction in a mechanically active organ, the gastrointestinal tract, is described. In the gut, mechanotransduction contributes to normal physiology and the development of motility disorders.
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10

Sun, Zhiqi, Shengzhen S. Guo, and Reinhard Fässler. "Integrin-mediated mechanotransduction." Journal of Cell Biology 215, no. 4 (November 8, 2016): 445–56. http://dx.doi.org/10.1083/jcb.201609037.

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Cells can detect and react to the biophysical properties of the extracellular environment through integrin-based adhesion sites and adapt to the extracellular milieu in a process called mechanotransduction. At these adhesion sites, integrins connect the extracellular matrix (ECM) with the F-actin cytoskeleton and transduce mechanical forces generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhesion proteins that are collectively termed the “molecular clutch.” The transmission of forces across integrin-based adhesions establishes a mechanical reciprocity between the viscoelasticity of the ECM and the cellular tension. During mechanotransduction, force allosterically alters the functions of mechanosensitive proteins within adhesions to elicit biochemical signals that regulate both rapid responses in cellular mechanics and long-term changes in gene expression. Integrin-mediated mechanotransduction plays important roles in development and tissue homeostasis, and its dysregulation is often associated with diseases.
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11

Jaalouk, Diana E., and Jan Lammerding. "Mechanotransduction gone awry." Nature Reviews Molecular Cell Biology 10, no. 1 (January 2009): 63–73. http://dx.doi.org/10.1038/nrm2597.

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12

Goldmann, Wolfgang H. "Mechanotransduction in cells." Cell Biology International 36, no. 6 (May 9, 2012): 567–70. http://dx.doi.org/10.1042/cbi20120071.

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13

Shoham, Naama, and Amit Gefen. "Mechanotransduction in adipocytes." Journal of Biomechanics 45, no. 1 (January 2012): 1–8. http://dx.doi.org/10.1016/j.jbiomech.2011.10.023.

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14

Duscher, Dominik, Zeshaan N. Maan, Victor W. Wong, Robert C. Rennert, Michael Januszyk, Melanie Rodrigues, Michael Hu, et al. "Mechanotransduction and fibrosis." Journal of Biomechanics 47, no. 9 (June 2014): 1997–2005. http://dx.doi.org/10.1016/j.jbiomech.2014.03.031.

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15

Ibar, Consuelo, and Kenneth D. Irvine. "Rapping about Mechanotransduction." Developmental Cell 46, no. 6 (September 2018): 678–79. http://dx.doi.org/10.1016/j.devcel.2018.09.007.

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16

Tsunozaki, Makoto, and Diana M. Bautista. "Mammalian somatosensory mechanotransduction." Current Opinion in Neurobiology 19, no. 4 (August 2009): 362–69. http://dx.doi.org/10.1016/j.conb.2009.07.008.

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17

Chukkapalli, Sasanka S., and Tanmay P. Lele. "Periodontal cell mechanotransduction." Open Biology 8, no. 9 (September 2018): 180053. http://dx.doi.org/10.1098/rsob.180053.

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The periodontium is a structurally and functionally complex tissue that facilitates the anchorage of teeth in jaws. The periodontium consists of various cell types including stem cells, fibroblasts and epithelial cells. Cells of the periodontium are constantly exposed to mechanical stresses generated by biological processes such as the chewing motions of teeth, by flows generated by tongue motions and by forces generated by implants. Mechanical stresses modulate the function of cells in the periodontium, and may play a significant role in the development of periodontal disease. Here, we review the literature on the effect of mechanical forces on periodontal cells in health and disease with an emphasis on molecular and cellular mechanisms.
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18

Katsumi, Akira, A. Wayne Orr, Eleni Tzima, and Martin Alexander Schwartz. "Integrins in Mechanotransduction." Journal of Biological Chemistry 279, no. 13 (February 11, 2004): 12001–4. http://dx.doi.org/10.1074/jbc.r300038200.

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19

Chin, LiKang, Yuntao Xia, Dennis E. Discher, and Paul A. Janmey. "Mechanotransduction in cancer." Current Opinion in Chemical Engineering 11 (February 2016): 77–84. http://dx.doi.org/10.1016/j.coche.2016.01.011.

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20

Ingber, Donald E. "Tensegrity and mechanotransduction." Journal of Bodywork and Movement Therapies 12, no. 3 (July 2008): 198–200. http://dx.doi.org/10.1016/j.jbmt.2008.04.038.

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21

Martinac, Boris, and Andrew R. Battle. "Biophysics of Mechanotransduction." European Biophysics Journal 44, no. 7 (August 28, 2015): 499–501. http://dx.doi.org/10.1007/s00249-015-1070-5.

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22

Ross, Tyler D., Brian G. Coon, Sanguk Yun, Nicolas Baeyens, Keiichiro Tanaka, Mingxing Ouyang, and Martin A. Schwartz. "Integrins in mechanotransduction." Current Opinion in Cell Biology 25, no. 5 (October 2013): 613–18. http://dx.doi.org/10.1016/j.ceb.2013.05.006.

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23

Orr, A. Wayne, Brian P. Helmke, Brett R. Blackman, and Martin A. Schwartz. "Mechanisms of Mechanotransduction." Developmental Cell 10, no. 1 (January 2006): 11–20. http://dx.doi.org/10.1016/j.devcel.2005.12.006.

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24

Orr, A. Wayne, Brian P. Helmke, Brett R. Blackman, and Martin A. Schwartz. "Mechanisms of Mechanotransduction." Developmental Cell 10, no. 3 (March 2006): 407. http://dx.doi.org/10.1016/j.devcel.2006.02.015.

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25

Chetambath, Ravindran, and Nithya Ravindran. "Mechanotransduction in fibrosis." Journal of Advanced Lung Health 3, no. 2 (2023): 79. http://dx.doi.org/10.4103/jalh.jalh_1_23.

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26

Robertson, Shaun N., Paul Campsie, Peter G. Childs, Fiona Madsen, Hannah Donnelly, Fiona L. Henriquez, William G. Mackay, et al. "Control of cell behaviour through nanovibrational stimulation: nanokicking." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 376, no. 2120 (April 16, 2018): 20170290. http://dx.doi.org/10.1098/rsta.2017.0290.

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Mechanical signals are ubiquitous in our everyday life and the process of converting these mechanical signals into a biological signalling response is known as mechanotransduction. Our understanding of mechanotransduction, and its contribution to vital cellular responses, is a rapidly expanding field of research involving complex processes that are still not clearly understood. The use of mechanical vibration as a stimulus of mechanotransduction, including variation of frequency and amplitude, allows an alternative method to control specific cell behaviour without chemical stimulation (e.g. growth factors). Chemical-independent control of cell behaviour could be highly advantageous for fields including drug discovery and clinical tissue engineering. In this review, a novel technique is described based on nanoscale sinusoidal vibration. Using finite-element analysis in conjunction with laser interferometry, techniques that are used within the field of gravitational wave detection, optimization of apparatus design and calibration of vibration application have been performed. We further discuss the application of nanovibrational stimulation, or ‘nanokicking’, to eukaryotic and prokaryotic cells including the differentiation of mesenchymal stem cells towards an osteoblast cell lineage. Mechanotransductive mechanisms are discussed including mediation through the Rho-A kinase signalling pathway. Optimization of this technique was first performed in two-dimensional culture using a simple vibration platform with an optimal frequency and amplitude of 1 kHz and 22 nm. A novel bioreactor was developed to scale up cell production, with recent research demonstrating that mesenchymal stem cell differentiation can be efficiently triggered in soft gel constructs. This important step provides first evidence that clinically relevant (three-dimensional) volumes of osteoblasts can be produced for the purpose of bone grafting, without complex scaffolds and/or chemical induction. Initial findings have shown that nanovibrational stimulation can also reduce biofilm formation in a number of clinically relevant bacteria. This demonstrates additional utility of the bioreactor to investigate mechanotransduction in other fields of research. This article is part of a discussion meeting issue ‘The promises of gravitational-wave astronomy’.
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27

Maurer, Melanie, and Jan Lammerding. "The Driving Force: Nuclear Mechanotransduction in Cellular Function, Fate, and Disease." Annual Review of Biomedical Engineering 21, no. 1 (June 4, 2019): 443–68. http://dx.doi.org/10.1146/annurev-bioeng-060418-052139.

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Cellular behavior is continuously affected by microenvironmental forces through the process of mechanotransduction, in which mechanical stimuli are rapidly converted to biochemical responses. Mounting evidence suggests that the nucleus itself is a mechanoresponsive element, reacting to cytoskeletal forces and mediating downstream biochemical responses. The nucleus responds through a host of mechanisms, including partial unfolding, conformational changes, and phosphorylation of nuclear envelope proteins; modulation of nuclear import/export; and altered chromatin organization, resulting in transcriptional changes. It is unclear which of these events present direct mechanotransduction processes and which are downstream of other mechanotransduction pathways. We critically review and discuss the current evidence for nuclear mechanotransduction, particularly in the context of stem cell fate, a largely unexplored topic, and in disease, where an improved understanding of nuclear mechanotransduction is beginning to open new treatment avenues. Finally, we discuss innovative technological developments that will allow outstanding questions in the rapidly growing field of nuclear mechanotransduction to be answered.
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28

Chopra, Anant, Erdem Tabdanov, Hersh Patel, Paul A. Janmey, and J. Yasha Kresh. "Cardiac myocyte remodeling mediated by N-cadherin-dependent mechanosensing." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 4 (April 2011): H1252—H1266. http://dx.doi.org/10.1152/ajpheart.00515.2010.

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Cell-to-cell adhesions are crucial in maintaining the structural and functional integrity of cardiac cells. Little is known about the mechanosensitivity and mechanotransduction of cell-to-cell interactions. Most studies of cardiac mechanotransduction and myofibrillogenesis have focused on cell-extracellular matrix (ECM)-specific interactions. This study assesses the direct role of intercellular adhesion, specifically that of N-cadherin-mediated mechanotransduction, on the morphology and internal organization of neonatal ventricular cardiac myocytes. The results show that cadherin-mediated cell attachments are capable of eliciting a cytoskeletal network response similar to that of integrin-mediated force response and transmission, affecting myofibrillar organization, myocyte shape, and cortical stiffness. Traction forces mediated by N-cadherin were shown to be comparable to those sustained by ECM. The directional changes in predicted traction forces as a function of imposed loads (gel stiffness) provide the added evidence that N-cadherin is a mechanoresponsive adhesion receptor. Strikingly, the mechanical sensitivity response (gain) in terms of the measured cell-spread area as a function of imposed load (adhesive substrate rigidity) was consistently higher for N-cadherin-coated surfaces compared with ECM protein-coated surfaces. In addition, the cytoskeletal architecture of myocytes on an N-cadherin adhesive microenvironment was characteristically different from that on an ECM environment, suggesting that the two mechanotransductive cell adhesion systems may play both independent and complementary roles in myocyte cytoskeletal spatial organization. These results indicate that cell-to-cell-mediated force perception and transmission are involved in the organization and development of cardiac structure and function.
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29

Alessandra, Galli, Marku Algerta, Marciani Paola, Schulte Carsten, Lenardi Cristina, Milani Paolo, Maffioli Elisa, Tedeschi Gabriella, and Perego Carla. "Shaping Pancreatic β-Cell Differentiation and Functioning: The Influence of Mechanotransduction." Cells 9, no. 2 (February 11, 2020): 413. http://dx.doi.org/10.3390/cells9020413.

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Embryonic and pluripotent stem cells hold great promise in generating β-cells for both replacing medicine and novel therapeutic discoveries in diabetes mellitus. However, their differentiation in vitro is still inefficient, and functional studies reveal that most of these β-like cells still fail to fully mirror the adult β-cell physiology. For their proper growth and functioning, β-cells require a very specific environment, the islet niche, which provides a myriad of chemical and physical signals. While the nature and effects of chemical stimuli have been widely characterized, less is known about the mechanical signals. We here review the current status of knowledge of biophysical cues provided by the niche where β-cells normally live and differentiate, and we underline the possible machinery designated for mechanotransduction in β-cells. Although the regulatory mechanisms remain poorly understood, the analysis reveals that β-cells are equipped with all mechanosensors and signaling proteins actively involved in mechanotransduction in other cell types, and they respond to mechanical cues by changing their behavior. By engineering microenvironments mirroring the biophysical niche properties it is possible to elucidate the β-cell mechanotransductive-regulatory mechanisms and to harness them for the promotion of β-cell differentiation capacity in vitro.
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30

Chang, Weipang, and Jianguo G. Gu. "Role of microtubules in Piezo2 mechanotransduction of mouse Merkel cells." Journal of Neurophysiology 124, no. 6 (December 1, 2020): 1824–31. http://dx.doi.org/10.1152/jn.00502.2020.

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Piezo2 channels are expressed in Merkel cells to mediate mechanotransduction leading to the sense of touch. Here we determined the role of microtubules in regulating Piezo2-mediated mechanotransduction in Merkel cells. Piezo2-mediated currents in Merkel cells are potentiated by microtubule stabilizer paclitaxel but reduced by microtubule destabilizer vincristine. Mechanically evoked afferent impulses are also enhanced by microtubule stabilizers and suppressed by microtubule destabilizers. Microtubules may play an essential role in Piezo2 mechanotransduction in Merkel cells.
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31

Stowers, Ryan, and Ovijit Chaudhuri. "Epigenetic regulation of mechanotransduction." Nature Biomedical Engineering 5, no. 1 (January 2021): 8–10. http://dx.doi.org/10.1038/s41551-020-00678-6.

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32

Shutova, Maria S., and Wolf-Henning Boehncke. "Mechanotransduction in Skin Inflammation." Cells 11, no. 13 (June 25, 2022): 2026. http://dx.doi.org/10.3390/cells11132026.

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In the process of mechanotransduction, the cells in the body perceive and interpret mechanical stimuli to maintain tissue homeostasis and respond to the environmental changes. Increasing evidence points towards dysregulated mechanotransduction as a pathologically relevant factor in human diseases, including inflammatory conditions. Skin is the organ that constantly undergoes considerable mechanical stresses, and the ability of mechanical factors to provoke inflammatory processes in the skin has long been known, with the Koebner phenomenon being an example. However, the molecular mechanisms and key factors linking mechanotransduction and cutaneous inflammation remain understudied. In this review, we outline the key players in the tissue’s mechanical homeostasis, the available data, and the gaps in our current understanding of their aberrant regulation in chronic cutaneous inflammation. We mainly focus on psoriasis as one of the most studied skin inflammatory diseases; we also discuss mechanotransduction in the context of skin fibrosis as a result of chronic inflammation. Even though the role of mechanotransduction in inflammation of the simple epithelia of internal organs is being actively studied, we conclude that the mechanoregulation in the stratified epidermis of the skin requires more attention in future translational research.
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33

Ingber, D. E. "Cellular Basis of Mechanotransduction." Biological Bulletin 194, no. 3 (June 1998): 323–27. http://dx.doi.org/10.2307/1543102.

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34

Adapala, Ravi K., Venkatesh Katari, Lakshminarayan Reddy Teegala, Sathwika Thodeti, Sailaja Paruchuri, and Charles K. Thodeti. "TRPV4 Mechanotransduction in Fibrosis." Cells 10, no. 11 (November 6, 2021): 3053. http://dx.doi.org/10.3390/cells10113053.

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Fibrosis is an irreversible, debilitating condition marked by the excessive production of extracellular matrix and tissue scarring that eventually results in organ failure and disease. Differentiation of fibroblasts to hypersecretory myofibroblasts is the key event in fibrosis. Although both soluble and mechanical factors are implicated in fibroblast differentiation, much of the focus is on TGF-β signaling, but to date, there are no specific drugs available for the treatment of fibrosis. In this review, we describe the role for TRPV4 mechanotransduction in cardiac and lung fibrosis, and we propose TRPV4 as an alternative therapeutic target for fibrosis.
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35

Porshneva, Kseniia, and Guillaume Montagnac. "Mechanotransduction mediated by microtubules." Nature Materials 21, no. 3 (October 18, 2021): 271–72. http://dx.doi.org/10.1038/s41563-021-01120-1.

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36

Scott, Alexander, Karim M. Khan, Vincent Duronio, and David A. Hart. "Mechanotransduction in Human Bone." Sports Medicine 38, no. 2 (2008): 139–60. http://dx.doi.org/10.2165/00007256-200838020-00004.

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37

Morgan, Elise F., Ryan E. Gleason, Lauren N. M. Hayward, Pui L. Leong, and Kristy T. Salisbury Palomares. "Mechanotransduction and Fracture Repair." Journal of Bone and Joint Surgery-American Volume 90, Suppl 1 (February 2008): 25–30. http://dx.doi.org/10.2106/jbjs.g.01164.

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38

Liu, Xiaowei, and Fumihiko Nakamura. "Mechanotransduction, nanotechnology, and nanomedicine." Journal of Biomedical Research 1 (2020): 1. http://dx.doi.org/10.7555/jbr.34.20200063.

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39

Burkholder, Thomas, J. "Mechanotransduction in skeletal muscle." Frontiers in Bioscience 12, no. 1 (2007): 174. http://dx.doi.org/10.2741/2057.

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40

Nakamura, Fumihiko. "Mechanotransduction in blood cells." Blood and Genomics 1, no. 1 (2017): 1–9. http://dx.doi.org/10.46701/apjbg.20170117017.

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41

Robling, Alexander, and Charles H. Turner. "Osteocytic Regulation of Mechanotransduction." Medicine & Science in Sports & Exercise 39, Supplement (May 2007): 33. http://dx.doi.org/10.1249/01.mss.0000272183.71742.7a.

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42

LAMMERDING, JAN, ROGER D. KAMM, and RICHARD T. LEE. "Mechanotransduction in Cardiac Myocytes." Annals of the New York Academy of Sciences 1015, no. 1 (May 2004): 53–70. http://dx.doi.org/10.1196/annals.1302.005.

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43

Sugden, Peter H. "Mechanotransduction in Cardiomyocyte Hypertrophy." Circulation 103, no. 10 (March 13, 2001): 1375–77. http://dx.doi.org/10.1161/01.cir.103.10.1375.

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44

Young, Roger C., and Gabriela Goloman. "Mechanotransduction in Rat Myometrium." Reproductive Sciences 18, no. 1 (August 16, 2010): 64–69. http://dx.doi.org/10.1177/1933719110379637.

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45

Turner, Charles H. "Mechanotransduction in skeletal cells." Current Opinion in Orthopaedics 13, no. 5 (October 2002): 363–67. http://dx.doi.org/10.1097/00001433-200210000-00006.

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46

Tschumperlin, Daniel J. "Matrix, Mesenchyme, and Mechanotransduction." Annals of the American Thoracic Society 12, Supplement 1 (March 2015): S24—S29. http://dx.doi.org/10.1513/annalsats.201407-320mg.

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47

Leckband, D. E., and J. de Rooij. "Cadherin Adhesion and Mechanotransduction." Annual Review of Cell and Developmental Biology 30, no. 1 (October 11, 2014): 291–315. http://dx.doi.org/10.1146/annurev-cellbio-100913-013212.

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48

Shafrir, Yinon, and Gabor Forgacs. "Mechanotransduction through the cytoskeleton." American Journal of Physiology-Cell Physiology 282, no. 3 (March 1, 2002): C479—C486. http://dx.doi.org/10.1152/ajpcell.00394.2001.

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We constructed a model cytoskeleton to investigate the proposal that this interconnected filamentous structure can act as a mechano- and signal transducer. The model cytoskeleton is composed of rigid rods representing actin filaments, which are connected with springs representing cross-linker molecules. The entire mesh is placed in viscous cytoplasm. The model eukaryotic cell is submitted to either shock wave-like or periodic mechanical perturbations at its membrane. We calculated the efficiency of this network to transmit energy to the nuclear wall as a function of cross-linker stiffness, cytoplasmic viscosity, and external stimulation frequency. We found that the cytoskeleton behaves as a tunable band filter: for given linker molecules, energy transmission peaks in a narrow range of stimulation frequencies. Most of the normal modes of the network are spread over the same frequency range. Outside this range, signals are practically unable to reach their destination. Changing the cellular ratios of linker molecules with different elastic characteristics can control the allowable frequency range and, with it, the efficiency of mechanotransduction.
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49

Goldmann, Wolfgang H. "Mechanotransduction and focal adhesions." Cell Biology International 36, no. 7 (June 8, 2012): 649–52. http://dx.doi.org/10.1042/cbi20120184.

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50

Williams, Erin R. "The basics of mechanotransduction." Science Signaling 11, no. 556 (November 13, 2018): eaau2223. http://dx.doi.org/10.1126/scisignal.aau2223.

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You might also be interested in the bibliographies on the topic 'Mechanotransduction' for other source types:
Dissertations / Theses Books
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