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Journal articles on the topic 'Structural remodeling'

To see the other types of publications on this topic, follow the link: Structural remodeling.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Corradi, Domenico, Sergio Callegari, Roberta Maestri, Stefano Benussi, and Ottavio Alfieri. "Structural remodeling in atrial fibrillation." Nature Clinical Practice Cardiovascular Medicine 5, no. 12 (October 14, 2008): 782–96. http://dx.doi.org/10.1038/ncpcardio1370.

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2

Irvin, Charles G. "Chronic Rhinosinusitis and Structural Remodeling." American Journal of Respiratory Cell and Molecular Biology 57, no. 3 (September 2017): 265–66. http://dx.doi.org/10.1165/rcmb.2017-0152ed.

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3

Cohn, Jay N. "Global structural ventricular remodeling: Summation." Journal of Cardiac Failure 8, no. 6 (December 2002): S269—S270. http://dx.doi.org/10.1054/jcaf.2002.129265.

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4

Harrigan, Timothy P., and James J. Hamilton. "Bone remodeling and structural optimization." Journal of Biomechanics 27, no. 3 (March 1994): 323–28. http://dx.doi.org/10.1016/0021-9290(94)90008-6.

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5

Ozawa, Hidehiro. "Fine Structural Aspects on Bone Remodeling." Nihon Hotetsu Shika Gakkai Zasshi 42, no. 3 (1998): 359–68. http://dx.doi.org/10.2186/jjps.42.359.

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6

Weber, Kaarl T., Yao Sun, and Jack P. M. Cleutjens. "Structural Remodeling of the Myocardium Postinfarction." Cardiology in Review 3, no. 1 (January 1995): 53. http://dx.doi.org/10.1097/00045415-199501000-00006.

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7

Zile, Michael R. "Structural components of cardiomyocyte remodeling: Summation." Journal of Cardiac Failure 8, no. 6 (December 2002): S311—S313. http://dx.doi.org/10.1054/jcaf.2002.129273.

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8

Kakauridze, N., Z. Tsagareli, and L. Gogiashvili. "Experimental atherosclerosis and lung structural remodeling." Atherosclerosis 275 (August 2018): e126. http://dx.doi.org/10.1016/j.atherosclerosis.2018.06.362.

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9

Volokh, O. I., N. I. Derkacheva, V. M. Studitsky, and O. S. Sokolova. "Structural studies of chromatin remodeling factors." Molecular Biology 50, no. 6 (November 2016): 812–22. http://dx.doi.org/10.1134/s0026893316060212.

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10

Sun, Xiaonan, Jalen Alford, and Hongyu Qiu. "Structural and Functional Remodeling of Mitochondria in Cardiac Diseases." International Journal of Molecular Sciences 22, no. 8 (April 17, 2021): 4167. http://dx.doi.org/10.3390/ijms22084167.

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Mitochondria undergo structural and functional remodeling to meet the cell demand in response to the intracellular and extracellular stimulations, playing an essential role in maintaining normal cellular function. Merging evidence demonstrated that dysregulation of mitochondrial remodeling is a fundamental driving force of complex human diseases, highlighting its crucial pathophysiological roles and therapeutic potential. In this review, we outlined the progress of the molecular basis of mitochondrial structural and functional remodeling and their regulatory network. In particular, we summarized the latest evidence of the fundamental association of impaired mitochondrial remodeling in developing diverse cardiac diseases and the underlying mechanisms. We also explored the therapeutic potential related to mitochondrial remodeling and future research direction. This updated information would improve our knowledge of mitochondrial biology and cardiac diseases’ pathogenesis, which would inspire new potential strategies for treating these diseases by targeting mitochondria remodeling.

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11

Ma, Jie, Xu-Yun Hua, Mou-Xiong Zheng, Jia-Jia Wu, Bei-Bei Huo, Xiang-Xin Xing, Wei Ding, and Jian-Guang Xu. "Structural remodeling secondary to functional remodeling in advanced-stage peripheral facial neuritis." Neurological Sciences 41, no. 9 (March 23, 2020): 2453–60. http://dx.doi.org/10.1007/s10072-020-04325-5.

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12

Naning, Roni, and MTS Darmawan. "Airway remodeling in asthma." Paediatrica Indonesiana 41, no. 3 (June 30, 2001): 125. http://dx.doi.org/10.14238/pi41.3.2001.125-131.

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Airway remodeling is the term given to a series of structural changes characterized by chronic, irreversible airway obstruction. Structural changes in the airway wall caused by chronic inflammation of asthma. Evidence for asthma airway remodeling demonstrating an accelerated decline of lung function that cannot be completely reversed with therapy. Combination therapy produced at least as much protection against inflammation as theuse of the higher dose of the inhaled corticosteroid.

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13

Fujita, Morihisa. "Structural Remodeling and Shedding of GPI-Anchors." Trends in Glycoscience and Glycotechnology 31, no. 181 (July 25, 2019): SE71—SE73. http://dx.doi.org/10.4052/tigg.1934.2se.

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14

Fujita, Morihisa. "Structural Remodeling and Shedding of GPI-Anchors." Trends in Glycoscience and Glycotechnology 31, no. 181 (July 25, 2019): SJ71—SJ73. http://dx.doi.org/10.4052/tigg.1934.2sj.

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15

Zhang, Yan, Xiaoyun Pang, Jian Li, Jiashu Xu, Victor W. Hsu, and Fei Sun. "Structural insights into membrane remodeling by SNX1." Proceedings of the National Academy of Sciences 118, no. 10 (March 3, 2021): e2022614118. http://dx.doi.org/10.1073/pnas.2022614118.

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The sorting nexin (SNX) family of proteins deform the membrane to generate transport carriers in endosomal pathways. Here, we elucidate how a prototypic member, SNX1, acts in this process. Performing cryoelectron microscopy, we find that SNX1 assembles into a protein lattice that consists of helical rows of SNX1 dimers wrapped around tubular membranes in a crosslinked fashion. We also visualize the details of this structure, which provides a molecular understanding of how various parts of SNX1 contribute to its ability to deform the membrane. Moreover, we have compared the SNX1 structure with a previously elucidated structure of an endosomal coat complex formed by retromer coupled to a SNX, which reveals how the molecular organization of the SNX in this coat complex is affected by retromer. The comparison also suggests insight into intermediary stages of assembly that results in the formation of the retromer-SNX coat complex on the membrane.

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16

Fukuda, Yuh, Hiroshi Mochimaru, Yasuhiro Terasaki, Masashi Kawamoto, and Shoji Kudoh. "Mechanism of Structural Remodeling in Pulmonary Fibrosis." Chest 120, no. 1 (July 2001): S41—S43. http://dx.doi.org/10.1378/chest.120.1_suppl.s41.

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17

Siddiqui, Sana, and James G. Martin. "Structural aspects of airway remodeling in asthma." Current Allergy and Asthma Reports 8, no. 6 (November 2008): 540–47. http://dx.doi.org/10.1007/s11882-008-0098-3.

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18

Burstein, Brett, and Stanley Nattel. "Atrial Structural Remodeling as an Antiarrhythmic Target." Journal of Cardiovascular Pharmacology 52, no. 1 (July 2008): 4–10. http://dx.doi.org/10.1097/fjc.0b013e3181668057.

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19

Vandooren, Bernard, Nataliya Yeremenko, Troy Noordenbos, Johannes Bras, Paul P. Tak, and Dominique Baeten. "Mediators of structural remodeling in peripheral spondylarthritis." Arthritis & Rheumatism 60, no. 12 (December 2009): 3534–45. http://dx.doi.org/10.1002/art.27251.

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20

Rahman, Kaysar, Azhar Halik, Kahar Samsak, and Nurmamat Helil. "Structural Topology Optimization Using Turing Model." Advanced Materials Research 889-890 (February 2014): 595–99. http://dx.doi.org/10.4028/www.scientific.net/amr.889-890.595.

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In this paper firstly a new hypothetical model of bone remodeling based on bone bioactivity mechanism and Turing reaction-diffusion equations is presented. Secondly this model of bone remodeling is translated to material formation and resorption process of continuum structures, a new heuristic structural topology optimization is presented. Finally short cantilever beam problem, one of the widely used examples in structural topology optimization are carried out by using present method to confirm the validity of the proposed topology optimization method.

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21

Rahman, Kaysar, Nurmamat Helil, Rahmatjan Imin, and Mamtimin Geni. "Structural Topology Optimization Method Based on Bone Remodeling." Applied Mechanics and Materials 423-426 (September 2013): 1813–18. http://dx.doi.org/10.4028/www.scientific.net/amm.423-426.1813.

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Bone is a dynamic living tissue that undergoes continuous adaptation of its mass and structure in response to mechanical and biological environment demands. In this paper, we firstly propose a mathematical model based on cross-type reaction diffusion equations of bone adaptation during a remodeling cycle due to mechanical stimulus. The model captures qualitatively very well the bone adaptation and cell interactions during the bone remodeling. Secondly assuming the bone structure to be a self-optimizing biological material which maximizes its own structural stiffness, bone remodeling model coupled with finite element method by using the add and remove element a new topology optimization of continuum structure is presented. Two Numerical examples demonstrate that the proposed approach greatly improves numerical efficiency, compared with the others well known methods for structural topology optimization in open literatures.

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22

McEwen, B. S., A. M. Magarinos, and L. P. Reagan. "Structural plasticity and tianeptine: cellular and molecular targets." European Psychiatry 17, S3 (July 2002): 318s—330s. http://dx.doi.org/10.1016/s0924-9338(02)00650-8.

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SummaryThe hippocampal formation, a structure involved in declarative, spatial and contextual memory, undergoes atrophy in depressive illness along with impairment in cognitive function. Animal model studies have shown that the hippocampus is a particularly sensitive and vulnerable brain region that responds to stress and stress hormones. Studies on models of stress and glucocorticoid actions reveal that the hippocampus shows a considerable degree of structural plasticity in the adult brain. Stress suppresses neurogenesis of dentate gyrus granule neurons, and repeated stress causes remodeling of dendrites in the CA3 region, a region that is particularly important in memory processing. Both forms of structural remodeling of the hippocampus are mediated by adrenal steroids working in concert with excitatory amino acids (EAA) and N-methyl-D-aspartate (NMDA) receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures, head trauma, and ischemia, and alterations of calcium homeostasis that accompany age-related cognitive impairment. Tianeptine (tianeptine) is an effective antidepressant that prevents and even reverses the actions of stress and glucocorticoids on dendritic remodeling in an animal model of chronic stress. Multiple neurotransmitter systems contribute to dendritic remodeling, including EAA, serotonin, and gamma-aminobutyric acid (GABA), working synergistically with glucocorticoids. This review summarizes findings on neurochemical targets of adrenal steroid actions that may explain their role in the remodeling process. In studying these actions, we hope to better understand the molecular and cellular targets of action of tianeptine in relation to its role in influencing structural plasticity of the hippocampus.

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23

Durmowicz, Anthony G., and Kurt R. Stenmark. "Mechanisms of Structural Remodeling in Chronic Pulmonary Hypertension." Pediatrics in Review 20, no. 11 (November 1999): e91-e102. http://dx.doi.org/10.1542/pir.20-11-e91.

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24

Durmowicz, Anthony G., and Kurt R. Stenmark. "Mechanisms of Structural Remodeling in Chronic Pulmonary Hypertension." Pediatrics In Review 20, no. 11 (November 1, 1999): e91-e102. http://dx.doi.org/10.1542/pir.20.11.e91.

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25

D'Andrea, Antonello, Andrè La Gerche, Enrica Golia, Arco J. Teske, Eduardo Bossone, Maria Giovanna Russo, Raffaele Calabrò, and Aaron L. Baggish. "Right Heart Structural and Functional Remodeling in Athletes." Echocardiography 32 (September 19, 2014): S11—S22. http://dx.doi.org/10.1111/echo.12226.

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26

Müller, C. W., C. R. Clapier, C. Fernández-Tornero, U. Steuerwald, T. Grüne, and I. Gutsche. "Structural studies of the nucleosome remodeling factor CHRAC." Acta Crystallographica Section A Foundations of Crystallography 62, a1 (August 6, 2006): s21. http://dx.doi.org/10.1107/s0108767306099570.

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27

Huang, Shiyuan, Xiaona Wang, Xinmei Wu, Jiale Yu, JinJing Li, Xiaoyuan Huang, Chunfang Zhu, and Hongshan Ge. "Yap regulates mitochondrial structural remodeling during myoblast differentiation." American Journal of Physiology-Cell Physiology 315, no. 4 (October 1, 2018): C474—C484. http://dx.doi.org/10.1152/ajpcell.00112.2018.

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Yes-associated protein (Yap) is a core transcriptional coactivator in the downstream Hippo pathway that regulates cell proliferation and tissue growth. However, its role in the regulation of myoblast differentiation remains unclear. Regulation of mitochondrial networks by dynamin-related protein 1 (Drp1) and mitofusion 2 (Mfn2) is crucial for the activation of myoblast differentiation. In the present study, we investigated the interplay between the Hippo/Yap pathway and protein contents of Mfn2 and Drp1 during myoblast differentiation. The Hippo/Yap pathway was inactivated at the early stage of myoblast differentiation due to the decreased ratio of phosphorylated mammalian sterile 20 kinases 1/2 (p-Mst1/2) to Mst1/2, phosphorylated large tumor suppressor 1 (p-Lats1) to Lats1, and phosphorylated Yap (serine 112, p-Yap S112) to Yap, which resulted in the translocation of Yap from cytoplasm to nucleus, increased protein content of Drp1, and mitochondrial fission events. Downregulation of Yap inhibited myoblast differentiation and decreased the content of Drp1, which resulted in elongated mitochondria, fused mitochondrial networks, and collapsed mitochondrial membrane potential. Together, our data indicate that inactivation of the Hippo/Yap pathway could induce mitochondrial fission by promoting Drp1 content at the early stage of myoblast differentiation.

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28

Patel, Kiran Haresh Kumar, Timothy Nicholas Jones, Susanne Sattler, Justin C. Mason, and Fu Siong Ng. "Proarrhythmic electrophysiological and structural remodeling in rheumatoid arthritis." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 5 (November 1, 2020): H1008—H1020. http://dx.doi.org/10.1152/ajpheart.00401.2020.

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Chronic inflammatory disorders, including rheumatoid arthritis (RA), are associated with a twofold increase in the incidence of sudden cardiac death (SCD) compared with the healthy population. Although this is partly explained by an increased prevalence of coronary artery disease, growing evidence suggests that ischemia alone cannot completely account for the increased risk. The present review explores the mechanisms of cardiac electrophysiological remodeling in response to chronic inflammation in RA. In particular, it focuses on the roles of nonischemic structural remodeling, altered cardiac ionic currents, and autonomic nervous system dysfunction in ventricular arrhythmogenesis and SCD. It also explores whether common genetic elements predispose to both RA and SCD. Finally, it evaluates the potential dual effects of disease-modifying therapy in both diminishing and promoting the risk of ventricular arrhythmias and SCD.

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29

Asturias, F. J., W. H. Chung, R. D. Kornberg, and Y. Lorch. "Structural analysis of the RSC chromatin-remodeling complex." Proceedings of the National Academy of Sciences 99, no. 21 (October 4, 2002): 13477–80. http://dx.doi.org/10.1073/pnas.162504299.

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30

Page, Kristen L., Gerard Celia, Giovanna Leddy, Douglas J. Taatjes, and George Osol. "Structural remodeling of rat uterine veins in pregnancy." American Journal of Obstetrics and Gynecology 187, no. 6 (December 2002): 1647–52. http://dx.doi.org/10.1067/mob.2002.127599.

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31

Sun, Si-jia, Jia-lu Yao, Lang-biao Xu, Qing Rui, Nan-nan Zhang, Min Chen, Yu-feng Jiang, Hua-jia Yang, and Ya-feng Zhou. "Retraction Note: Cardiac structural remodeling in hypertensive cardiomyopathy." Hypertension Research 41, no. 12 (October 11, 2018): 1073. http://dx.doi.org/10.1038/s41440-018-0097-2.

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32

Sun, Daniel, and Tatjana C. Jakobs. "Structural Remodeling of Astrocytes in the Injured CNS." Neuroscientist 18, no. 6 (October 7, 2011): 567–88. http://dx.doi.org/10.1177/1073858411423441.

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Astrocytes respond to all forms of CNS insult and disease by becoming reactive, a nonspecific but highly characteristic response that involves various morphological and molecular changes. Probably the most recognized aspect of reactive astrocytes is the formation of a glial scar that impedes axon regeneration. Although the reactive phenotype was first suggested more than 100 years ago based on morphological changes, the remodeling process is not well understood. We know little about the actual structure of a reactive astrocyte, how an astrocyte remodels during the progression of an insult, and how populations of these cells reorganize to form the glial scar. New methods of labeling astrocytes, along with transgenic mice, allow the complete morphology of reactive astrocytes to be visualized. Recent studies show that reactivity can induce a remarkable change in the shape of a single astrocyte, that not all astrocytes react in the same way, and that there is plasticity in the reactive response.

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33

Allessie, M. "Electrical, contractile and structural remodeling during atrial fibrillation." Cardiovascular Research 54, no. 2 (May 2002): 230–46. http://dx.doi.org/10.1016/s0008-6363(02)00258-4.

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34

Reddy, H. "Structural correlates of electrical remodeling in ventricular hypertrophy." Cardiovascular Research 58, no. 3 (June 1, 2003): 495–97. http://dx.doi.org/10.1016/s0008-6363(03)00369-9.

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35

Leonard, Bridget Louise, Bruce Henry Smaill, and Ian John LeGrice. "Structural Remodeling and Mechanical Function in Heart Failure." Microscopy and Microanalysis 18, no. 1 (January 18, 2012): 50–67. http://dx.doi.org/10.1017/s1431927611012438.

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AbstractThe cardiac extracellular matrix (ECM) is the three-dimensional scaffold that defines the geometry and muscular architecture of the cardiac chambers and transmits forces produced during the cardiac cycle throughout the heart wall. The cardiac ECM is an active system that responds to the stresses to which it is exposed and in the normal heart is adapted to facilitate efficient mechanical function. There are marked differences in the short- and medium-term changes in ventricular geometry and cardiac ECM that occur as a result of volume overload, hypertension, and ischemic cardiomyopathy. Despite this, there is a widespread view that a common remodeling “phenotype” governs the final progression to end-stage heart failure in different forms of heart disease. In this review article, we make the case that this interpretation is not consistent with the clinical and experimental data on the topic. We argue that there is a need for new theoretical and experimental models that will enable stresses acting on the ECM and resultant deformations to be estimated more accurately and provide better spatial resolution of local signaling mechanisms that are activated as a result. These developments are necessary to link the effects of structural remodeling with altered cardiac mechanical function.

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36

Armoundas, Antonis A., Richard Wu, George Juang, Eduardo Marbán, and Gordon F. Tomaselli. "Electrical and structural remodeling of the failing ventricle." Pharmacology & Therapeutics 92, no. 2-3 (November 2001): 213–30. http://dx.doi.org/10.1016/s0163-7258(01)00171-1.

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37

Casaclang-Verzosa, Grace, Bernard J. Gersh, and Teresa S. M. Tsang. "Structural and Functional Remodeling of the Left Atrium." Journal of the American College of Cardiology 51, no. 1 (January 2008): 1–11. http://dx.doi.org/10.1016/j.jacc.2007.09.026.

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38

Richmond, Timothy J., Kazuhiro Yamada, Tim Frouws, Brigitte Angst, and Kyoko Schimmele. "Structural Studies on the Chromatin Remodeling Factor ISW1a." Biophysical Journal 96, no. 3 (February 2009): 544a. http://dx.doi.org/10.1016/j.bpj.2008.12.2942.

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39

Chen, Jerry L., and Elly Nedivi. "Neuronal structural remodeling: is it all about access?" Current Opinion in Neurobiology 20, no. 5 (October 2010): 557–62. http://dx.doi.org/10.1016/j.conb.2010.06.002.

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40

Sun, D., M. Lye-Barthel, R. H. Masland, and T. C. Jakobs. "Structural Remodeling of Fibrous Astrocytes after Axonal Injury." Journal of Neuroscience 30, no. 42 (October 20, 2010): 14008–19. http://dx.doi.org/10.1523/jneurosci.3605-10.2010.

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41

New, David I., Alistair M. Chesser, Raj C. Thuraisingham, and Magdi M. Yaqoob. "Structural remodeling of resistance arteries in uremic hypertension." Kidney International 65, no. 5 (May 2004): 1818–25. http://dx.doi.org/10.1111/j.1523-1755.2004.00591.x.

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42

Sun, Si-jia, Jia-lu Yao, Lang-biao Xu, Qing Rui, Nan-nan Zhang, Min Chen, Yu-feng Jiang, Hua-jia Yang, and Ya-feng Zhou. "RETRACTED ARTICLE: Cardiac structural remodeling in hypertensive cardiomyopathy." Hypertension Research 40, no. 5 (December 22, 2016): 450–56. http://dx.doi.org/10.1038/hr.2016.169.

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43

Gaasch, William H., and Michael R. Zile. "Left Ventricular Structural Remodeling in Health and Disease." Journal of the American College of Cardiology 58, no. 17 (October 2011): 1733–40. http://dx.doi.org/10.1016/j.jacc.2011.07.022.

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44

He, Yaoyao, Bai Du, Huiting Fan, Jian Cao, Zi Wang Liu, Yonglie Zhao, Mingjing Zhao, Yizhou Zhao, Xin Zhao, and Xiangning Cui. "Beneficial Effects of Qili Qiangxin Capsule on Lung Structural Remodeling in Ischemic Heart Failure via TGF-β1/Smad3 Pathway." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/298631.

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Qili qiangxin (QL) capsule is a traditional Chinese medicine that is widely used for the treatment of patients with chronic heart failure (CHF) of all etiologies, although the exact mechanisms of action remain unclear. CHF leads to pulmonary vascular remodelling and thickening of the alveolar-capillary barrier that may be important mechanisms in the poor clinical outcome in patients with end-stage heart failure. We examined whether QL could improve lung injury in ischemic CHF by reducing lung remodeling. Rats with myocardial infarct received QL (1.0 g/kg/day) for 4 weeks. Echocardiographic and morphometric measurements were obtained followed by echocardiography, histological staining, and immunohistochemical analysis of lung sections. CHF caused significant lung structural remodeling evidenced by collagen deposition and thickening of the alveolar septa after myocardial infarct that were greatly improved by QL. Lung weight increased after infarct with no evidence of pulmonary edema and was normalized by QL. QL also reduced lung transforming growth factor-β1 (TGF-β1), p-Smad3, tumor necrosis factor-α(TNF-α), and Toll-like receptor-4 (TLR4) expression. Thus, QL reduces lung remodeling associated with CHF, mainly by suppressing the TGF-β1/Smad3 signaling pathway. The mechanism may also involve inhibition of TLR4 intracellular signaling.

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45

Prado, Adelina, Isbaal Ramos, Lindsay J. Frehlick, Arturo Muga, and Juan Ausió. "Nucleoplasmin: a nuclear chaperone." Biochemistry and Cell Biology 82, no. 4 (August 1, 2004): 437–45. http://dx.doi.org/10.1139/o04-042.

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In this article, we briefly review the structural and functional information currently available on nucleoplasmin. Special emphasis is placed on the discussion of the molecular mechanism involved in the sperm chromatin remodelling activity of this protein. A model is proposed based on current crystallographic data, recent biophysical and functional studies, as well as in the previously available information.Key words: nucleoplasmin, review, histone chaperone, sperm chromatin remodeling, nucleosome assembly.

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46

Naidich, A. M. "Left ventricular structural heterogeneity and myocardial remodelling." Bulletin of Siberian Medicine 5, no. 1 (March 30, 2006): 38–45. http://dx.doi.org/10.20538/1682-0363-2006-1-38-45.

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Aimed at studying interrelation between left ventricular (LV) structural heterogeneity and myocardial remodeling, we exa- mined a group pf subjects having coronary artery disease (CAD) of several severity degree. Based on three-dimensional reconstruc-tion of LV and using original analysis methods of esophageal ultrasound investigation data, standard parameters of myocardial re-modeling ( mean values of wall thickness and short axis LV radius, interrelations of long and short semi-axes, camera volume, myo-cardial mass and its relation to the wall thickness) were scored. The assessment of heterogeneity in LV regions was performed with space resolution 4x4 mm using parameters which are characteristic of heterogeneity of the wall thickness and curvature degree and also, scale of constitution of connective material by connective tissue. Correlation analysis performed between data of LV remodel-ing and its structural heterogeneity revealed strong correlation events studied in the heart. It proved that the higher myocardial re-modeling degree the lower heterogeneity of LV. It means that myocardial remodeling process in the setting of advancing CAD de-velops to decreased scale of LV structural heterogeneity. It is suggested that heterogeneity in normal heart serves as structural basis for myocardial remodeling.

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47

Mages, Christine, Heike Gampp, Pascal Syren, Ann-Kathrin Rahm, Florian André, Norbert Frey, Patrick Lugenbiel, and Dierk Thomas. "Electrical Ventricular Remodeling in Dilated Cardiomyopathy." Cells 10, no. 10 (October 15, 2021): 2767. http://dx.doi.org/10.3390/cells10102767.

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Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affecting electrophysiologic properties of ventricular cardiomyocytes. The dysregulation of ion channel expression has been associated with cardiomyopathy and with the development of arrhythmias. However, the underlying molecular signaling pathways are increasingly recognized. This review summarizes clinical and cellular electrophysiologic characteristics observed in dilated cardiomyopathy (DCM) with ionic and structural alterations at the ventricular level. Furthermore, potential translational strategies and therapeutic options are highlighted.

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48

Liu, Lei, Jianqiang Geng, Hongwei Zhao, Fengxiang Yun, Xiaoyu Wang, Sen Yan, Xue Ding, et al. "Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway." Cellular Physiology and Biochemistry 36, no. 5 (2015): 2039–50. http://dx.doi.org/10.1159/000430171.

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Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.

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Lujan, Heidi L., Hussein Janbaih, and Stephen E. DiCarlo. "Structural remodeling of the heart and its premotor cardioinhibitory vagal neurons following T5 spinal cord transection." Journal of Applied Physiology 116, no. 9 (May 1, 2014): 1148–55. http://dx.doi.org/10.1152/japplphysiol.01285.2013.

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Midthoracic spinal cord injury (SCI) is associated with enhanced cardiac sympathetic activity and reduced cardiac parasympathetic activity. The enhanced cardiac sympathetic activity is associated with sympathetic structural plasticity within the stellate ganglia, spinal cord segments T1–T4, and heart. However, changes to cardiac parasympathetic centers rostral to an experimental SCI are relatively unknown. Importantly, reduced vagal activity is a predictor of high mortality. Furthermore, this autonomic dysregulation promotes progressive left ventricular (LV) structural remodeling. Accordingly, we hypothesized that midthoracic spinal cord injury is associated with structural plasticity in premotor (preganglionic parasympathetic neurons) cardioinhibitory vagal neurons located within the nucleus ambiguus as well as LV structural remodeling. To test this hypothesis, dendritic arborization and morphology (cholera toxin B immunohistochemistry and Sholl analysis) of cardiac projecting premotor cardioinhibitory vagal neurons located within the nucleus ambiguus were determined in intact (sham transected) and thoracic level 5 transected (T5X) rats. In addition, LV chamber size, wall thickness, and collagen content (Masson trichrome stain and structural analysis) were determined. Midthoracic SCI was associated with structural changes within the nucleus ambiguus and heart. Specifically, following T5 spinal cord transection, there was a significant increase in cardiac parasympathetic preganglionic neuron dendritic arborization, soma area, maximum dendritic length, and number of intersections/animal. This parasympathetic structural remodeling was associated with a profound LV structural remodeling. Specifically, T5 spinal cord transection increased LV chamber area, reduced LV wall thickness, and increased collagen content. Accordingly, results document a dynamic interaction between the heart and its parasympathetic innervation.

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Wu, Guojie, Adam J. Quek, Tom T. Caradoc-Davies, Sue M. Ekkel, Blake Mazzitelli, James C. Whisstock, and Ruby H. P. Law. "Structural studies of plasmin inhibition." Biochemical Society Transactions 47, no. 2 (March 5, 2019): 541–57. http://dx.doi.org/10.1042/bst20180211.

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Abstract Plasminogen (Plg) is the zymogen form of the serine protease plasmin (Plm), and it plays a crucial role in fibrinolysis as well as wound healing, immunity, tissue remodeling and inflammation. Binding to the targets via the lysine-binding sites allows for Plg activation by plasminogen activators (PAs) present on the same target. Cellular uptake of fibrin degradation products leads to apoptosis, which represents one of the pathways for cross-talk between fibrinolysis and tissue remodeling. Therapeutic manipulation of Plm activity plays a vital role in the treatments of a range of diseases, whereas Plm inhibitors are used in trauma and surgeries as antifibrinolytic agents. Plm inhibitors are also used in conditions such as angioedema, menorrhagia and melasma. Here, we review the rationale for the further development of new Plm inhibitors, with a particular focus on the structural studies of the active site inhibitors of Plm. We compare the binding mode of different classes of inhibitors and comment on how it relates to their efficacy, as well as possible future developments.

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