New therapeutic targets for human placental angiogenesis diseases (Record no. 63876)

MARC details
000 -LEADER
fixed length control field 02807naaaa2200301uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/54618
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20220220040107.0
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 978-2-88919-461-2
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9782889194612
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.3389/978-2-88919-461-2
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 Carlos Alonso Escudero
Relationship auth
245 10 - TITLE STATEMENT
Title New therapeutic targets for human placental angiogenesis diseases
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Name of publisher, distributor, etc. Frontiers Media SA
Date of publication, distribution, etc. 2015
300 ## - PHYSICAL DESCRIPTION
Extent 1 electronic resource (113 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. A large number of publications have described impaired angiogenesis and vasculogenesis present in the feto-placental circulation after pregnancy diseases such as pre-eclamptic pregnancies, gestational diabetes, and intrauterine growth restriction, among others. Results suggest impaired secretion and activity of pro-angiogenic factors such as vascular endothelial growth factor (VEGF), interleukin 8 (IL-8), adenosine and nitric oxide, associates with compromised secretion and activity of anti-angiogenic factors such as soluble receptor of VEGF (sFlt-1), thrombospondin 2, endostatin among others. More recent evidences include the participation of endothelial progenitor cells (EPC), which circulating number is reduced infeto-placental circulation in pregnancies such as pre-eclampsia. Despite this knowledge, therapies for placental angiogenesis recovery during pathological pregnancies are far to be tested. However, from the cardiovascular field, it has been described the administration of EPC, alone or used as gene-transfer therapy; or it has been described the potential role of statins (HMGCoA inhibitors), or angiotensin-converter enzyme (ACE) inhibitors for enhancing angiogenesis. Finally, feto-placental tissue is an exceptional source of progenitor and stem cells, which could be used for treated other human diseases such as stroke, myocardial infarction, hypertension, or even cancer. In this research topic, authors highlight physiopatological and clinical importance of the impaired placental angiogenesis, and suggest potential targets for developing innovative therapies.
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
Use and reproduction rights https://creativecommons.org/licenses/by/4.0/
Source of term cc
-- https://creativecommons.org/licenses/by/4.0/
546 ## - LANGUAGE NOTE
Language note English
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term Angiogenesis
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term Placenta
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term therapy
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term fetal programming
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Uncontrolled term Pregnancy Diseases
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="http://journal.frontiersin.org/researchtopic/1892/new-therapeutic-targets-for-human-placental-angiogenesis-diseases">http://journal.frontiersin.org/researchtopic/1892/new-therapeutic-targets-for-human-placental-angiogenesis-diseases</a>
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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/20.500.12854/54618">https://directory.doabooks.org/handle/20.500.12854/54618</a>
Access status 0
Public note DOAB: description of the publication

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