Connexins, Pannexins, and Their Channels in Fibroproliferative Diseases

被引:0
作者
Bruno Cogliati
Gregory Mennecier
Joost Willebrords
Tereza Cristina Da Silva
Michaël Maes
Isabel Veloso Alves Pereira
Sara Crespo Yanguas
Francisco Javier Hernandez-Blazquez
Maria Lúcia Zaidan Dagli
Mathieu Vinken
机构
[1] University of São Paulo,Department of Pathology, School of Veterinary Medicine and Animal Science
[2] Vrije Universiteit Brussel,Department of In Vitro Toxicology and Dermato
[3] University of São Paulo,Cosmetology, Faculty of Medicine and Pharmacy
来源
The Journal of Membrane Biology | 2016年 / 249卷
关键词
Tissue repair; Wound healing; Fibrosis; Cellular communication; Fibrotic diseases;
D O I
暂无
中图分类号
学科分类号
摘要
Cellular and molecular mechanisms of wound healing, tissue repair, and fibrogenesis are established in different organs and are essential for the maintenance of function and tissue integrity after cell injury. These mechanisms are also involved in a plethora of fibroproliferative diseases or organ-specific fibrotic disorders, all of which are associated with the excessive deposition of extracellular matrix components. Fibroblasts, which are key cells in tissue repair and fibrogenesis, rely on communicative cellular networks to ensure efficient control of these processes and to prevent abnormal accumulation of extracellular matrix into the tissue. Despite the significant impact on human health, and thus the epidemiologic relevance, there is still no effective treatment for most fibrosis-related diseases. This paper provides an overview of current concepts and mechanisms involved in the participation of cellular communication via connexin-based pores as well as pannexin-based channels in the processes of tissue repair and fibrogenesis in chronic diseases. Understanding these mechanisms may contribute to the development of new therapeutic strategies to clinically manage fibroproliferative diseases and organ-specific fibrotic disorders.
引用
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页码:199 / 213
页数:14
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  • [1] Abdullah KM(1999)Cell-to-cell communication and expression of gap junctional proteins in human diabetic and nondiabetic skin fibroblasts: effects of basic fibroblast growth factor Endocrine 10 35-41
  • [2] Luthra G(2014)The connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes Front Cell Neurosci 8 306-482
  • [3] Bilski JJ(2012)The noncanonical functions of Cx43 in the heart J Membr Biol 245 477-24431
  • [4] Abdullah SA(2010)Pannexin1 and Pannexin2 channels show quaternary similarities to connexons and different oligomerization numbers from each other J Biol Chem 285 24420-1199
  • [5] Reynolds LP(2009)Cx43 contributes to TGF-beta signaling to regulate differentiation of cardiac fibroblasts into myofibroblasts Exp Cell Res 315 1190-149
  • [6] Redmer DA(2009)Targeting connexin 43 in diabetic wound healing: future perspectives J Postgrad Med 55 143-1200
  • [7] Grazul-Bilska AT(2013)Importance of Connexin-43 based gap junction in cirrhosis and acute-on-chronic liver failure J Hepatol 58 1194-716
  • [8] Abudara V(2004)The mammalian pannexin family is homologous to the invertebrate innexin gap junction proteins Genomics 83 706-114
  • [9] Bechberger J(2006)Cell–cell communication beyond connexins: the pannexin channels Physiology (Bethesda) 21 103-20777
  • [10] Freitas-Andrade M(2011)Pannexins in ischemia-induced neurodegeneration Proc Natl Acad Sci USA 108 20772-379