Ha Leal (UniversitCatholique de Louvain, Brussels, Belgium) and John Hanrahan (McGill University, Montreal, Canada) report exciting observations relating to the potential of numerous inhibitors in correcting the CF phenotype at the degree of ion transport and inflammation. Luigi Maiuriand collaborators (European Institute for Study in Cystic Fibrosis, San Raffaele Scientific Institute, Milan, Italy) propose to target the intracellular atmosphere so as to reestablish functional autophagy in CF epithelial cells. The third chapter is devoted to new molecules that have currently been developed or in improvement and in a position to rescue CFTR channel function by targeting mutant CFTR at the mRNA (Michael Wilschanski, Hadassah Hospitals- Hebrew University, Jerusalem, Israel) and/or at the protein (Nicoletta Pedemonte and Luis Galietta, Laboratorio di Genetica Molecolare, Istituto Giannina Gaslini Genova, Italy) levels. Finally, the Particular Subject is concluded by an in-depth critique by Christine Bear and collaborators (The Hospital for Sick Young children, Toronto, Canada). Importantly, the gaps in our knowledge concerning the mechanism of action of current correctors, the unmet must discover compounds which restore appropriate CFTR structure and function in CF affected tissues and new strategies for therapy improvement are discussed. We are convinced that we accomplished an incredibly fascinating Particular Subjects due to the outstanding contributions of all authors. We are specially grateful to the authors for having believed in this project and accepted to share their expertise. All of the manuscripts have been peer-reviewed and we would like to thank the specialists for assisting us to reach a problem of high regular.Received: 11 June 2013; accepted: 08 August 2013; published on the internet: 29 August 2013. Citation: Becq F and Chanson M (2013) Tactics to circumvent the CFTR defect in cystic fibrosis. Front. Pharmacol. 4:108. doi: ten.3389/fphar.2013.00108 This article was submitted to Pharmacology of Ion Channels and Channelopathies, a section of your journal Frontiers in Pharmacology. Copyright 2013 Becq and Chanson. This can be an open-access report distributed under the terms from the Inventive Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication within this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which doesn’t comply with these terms.www.frontiersin.orgAugust 2013 | Volume four | Post 108 |
Viewpoint SERIESTissue responses to ischemiaBrain tissue responses to ischemiaJin-Moo Lee, Margaret C.Acalabrutinib Grabb, Gregory J.Sulforhodamine 101 Zipfel, and Dennis W.PMID:36014399 ChoiCenter for the Study of Nervous Method Injury and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA Address correspondence to: Dennis W. Choi, Department of Neurology, Washington University College of Medicine, Campus Box 8111, 660 S. Euclid Avenue, St. Louis, Missouri 63110, USA. Telephone: (314) 362-9460; Fax: (314) 362-9462; E-mail: [email protected] brain is especially vulnerable to ischemia. Total interruption of blood flow towards the brain for only 5 minutes triggers the death of vulnerable neurons in several brain regions, whereas 200 minutes of ischemia is expected to kill cardiac myocytes or kidney cells. In element, the prominent vulnerability of brain tissue to ischemic harm refle.