MARC details
000 -LEADER |
fixed length control field |
03615naaaa2200325uu 4500 |
001 - CONTROL NUMBER |
control field |
https://directory.doabooks.org/handle/20.500.12854/54888 |
005 - DATE AND TIME OF LATEST TRANSACTION |
control field |
20220714175047.0 |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
International Standard Book Number |
978-2-88945-372-6 |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER |
International Standard Book Number |
9782889453726 |
024 7# - OTHER STANDARD IDENTIFIER |
Standard number or code |
10.3389/978-2-88945-372-6 |
Terms of availability |
doi |
041 0# - LANGUAGE CODE |
Language code of text/sound track or separate title |
English |
042 ## - AUTHENTICATION CODE |
Authentication code |
dc |
100 1# - MAIN ENTRY--PERSONAL NAME |
Personal name |
Timothy D. Hewitson |
Relator code |
auth |
9 (RLIN) |
1592797 |
245 10 - TITLE STATEMENT |
Title |
Novel Therapeutic Targets and Emerging Treatments for Fibrosis |
260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) |
Name of publisher, distributor, etc |
Frontiers Media SA |
Date of publication, distribution, etc |
2018 |
300 ## - PHYSICAL DESCRIPTION |
Extent |
1 electronic resource (162 p.) |
506 0# - RESTRICTIONS ON ACCESS NOTE |
Terms governing access |
Open Access |
Source of term |
star |
Standardized terminology for access restriction |
Unrestricted online access |
520 ## - SUMMARY, ETC. |
Summary, etc |
For decades we have known that the overgrowth, hardening and scarring of tissues (so-called fibrosis) represents the final common pathway and best histological predictor of disease progression in most organs. Fibrosis is the culmination of both excess extracellular matrix deposition due to ongoing or severe injury, and a failure to regenerate. An inadequate wound repair process ultimately results in organ failure through a loss of function, and is therefore a major cause of morbidity and mortality in disease affecting both multiple and individual organs.Whilst the pathology of fibrosis and its significance are well understood, until recently we have known little about its molecular regulation. Current therapies are often indirect and non-specific, and only slow progression by a matter of months. The recent identification of novel therapeutic targets, and the development of new treatment strategies based on them, offers the exciting prospect of more efficacious therapies to treat this debilitating disorder.This Research Topic therefore compromises several up-to-date mini-reviews on currently known and emerging therapeutic targets for fibrosis including: the Transforming Growth Factor (TGF)-family; epigenetic factors; Angiotensin II type 2 (AT2) receptors; mineralocorticoid receptors; adenosine receptors; caveolins; and the sphingosine kinase/sphingosine 1-phosphate and notch signaling pathways. In each case, mechanistic insights into how each of these factors contribute to regulating fibrosis progression are described, along with how they can be targeted (by existing drugs, small molecules or other mimetics) to prevent and/or reverse fibrosis and its contribution to tissue dysfunction and failure. Two additional reviews will discuss various anti-fibrotic therapies that have demonstrated efficacy at the experimental level, but are not yet clinically approved; and the therapeutic potential vs limitations of stem cell-based therapies for reducing fibrosis while facilitating tissue repair. Finally, this Research Topic concludes with a clinical perspective of various anti-fibrotic therapies for cardiovascular disease (CVD), outlining limitations of currently used therapies, the pipeline of anti-fibrotics for CVD and why so many anti-fibrotic drugs have failed at the clinical level. |
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE |
Terms governing use and reproduction |
Creative Commons |
-- |
https://creativecommons.org/licenses/by/4.0/ |
-- |
cc |
-- |
https://creativecommons.org/licenses/by/4.0/ |
546 ## - LANGUAGE NOTE |
Language note |
English |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
treatment strategies |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
Fibrosis |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
pharmacology |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
collagen |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
fibrogenesis |
653 ## - INDEX TERM--UNCONTROLLED |
Uncontrolled term |
therapeutic targets |
700 1# - ADDED ENTRY--PERSONAL NAME |
Personal name |
Chrishan S. Samuel |
Relator code |
auth |
9 (RLIN) |
1592798 |
856 40 - ELECTRONIC LOCATION AND ACCESS |
Host name |
www.oapen.org |
Uniform Resource Identifier |
<a href="https://www.frontiersin.org/research-topics/5288/novel-therapeutic-targets-and-emerging-treatments-for-fibrosis">https://www.frontiersin.org/research-topics/5288/novel-therapeutic-targets-and-emerging-treatments-for-fibrosis</a> |
-- |
0 |
Public note |
DOAB: download the publication |
856 40 - ELECTRONIC LOCATION AND ACCESS |
Host name |
www.oapen.org |
Uniform Resource Identifier |
<a href="https://directory.doabooks.org/handle/20.500.12854/54888">https://directory.doabooks.org/handle/20.500.12854/54888</a> |
-- |
0 |
Public note |
DOAB: description of the publication |