Loading…

Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms

Reactive oxygen species are the reactive molecules that are derived from molecular oxygen and play an important role as redox signaling molecules to confer cardioprotection. Various scientists have demonstrated the key role of redox signaling in cardioprotection by showing a transient increase in th...

Full description

Saved in:
Bibliographic Details
Published in:European journal of pharmacology 2017-08, Vol.809, p.151-155
Main Authors: singh, Lovedeep, Randhawa, Puneet Kaur, Singh, Nirmal, Jaggi, Amteshwar Singh
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3
cites cdi_FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3
container_end_page 155
container_issue
container_start_page 151
container_title European journal of pharmacology
container_volume 809
creator singh, Lovedeep
Randhawa, Puneet Kaur
Singh, Nirmal
Jaggi, Amteshwar Singh
description Reactive oxygen species are the reactive molecules that are derived from molecular oxygen and play an important role as redox signaling molecules to confer cardioprotection. Various scientists have demonstrated the key role of redox signaling in cardioprotection by showing a transient increase in their levels during remote ischemic preconditioning (RIPC) phase. The transient increase in reactive oxygen species levels during remote preconditioning phase may take place either through activation of KATP channels or through increased nitric oxide (NO) production. A transient increase in reactive oxygen species during preconditioning may also increase the expression of heat shock proteins (HSP), the level of antioxidant enzymes and decrease the expression of inflammatory genes (Egr-1) during ischemia-reperfusion phase to confer cardioprotection. The present review describes the role of redox signaling in RIPC-induced cardioprotective effect with possible mechanisms.
doi_str_mv 10.1016/j.ejphar.2017.05.033
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1900833021</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0014299917303515</els_id><sourcerecordid>1900833021</sourcerecordid><originalsourceid>FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3</originalsourceid><addsrcrecordid>eNp9kMtKxDAUhoMoOl7eQCRLN60nSdM2LgQRbyAIouuQSU6dDNN0TDqDvr0ZRl26Oovz_efyEXLKoGTA6ot5ifPlzMSSA2tKkCUIsUMmrG1UAQ3ju2QCwKqCK6UOyGFKcwCQist9csBbyWsh2gnBF3TDJ03-PZiFD-_UBxqxH0akPtkZ9t7SZUQ7BOdHP4SMFD64lUVHrYnOD8uYYbvpXdLbtXcYLCZqgqM92pkJPvXpmOx1ZpHw5Kcekbe729ebh-Lp-f7x5vqpsKLmY6GUdMzITliDhvHKOMOlrJlVnUDW1HXluhZVXVVT10xROGx5wzveQC1Q4lQckfPt3HzUxwrTqPv8BS4WJuCwSpopgFYI4Cyj1Ra1cUgpYqeX0fcmfmkGeiNYz_VWsN4I1iB1FpxjZz8bVtMe3V_o12gGrrYA5j_XHqNO1m-cOJ81jtoN_v8N30EnkGw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1900833021</pqid></control><display><type>article</type><title>Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms</title><source>ScienceDirect Freedom Collection 2022-2024</source><creator>singh, Lovedeep ; Randhawa, Puneet Kaur ; Singh, Nirmal ; Jaggi, Amteshwar Singh</creator><creatorcontrib>singh, Lovedeep ; Randhawa, Puneet Kaur ; Singh, Nirmal ; Jaggi, Amteshwar Singh</creatorcontrib><description>Reactive oxygen species are the reactive molecules that are derived from molecular oxygen and play an important role as redox signaling molecules to confer cardioprotection. Various scientists have demonstrated the key role of redox signaling in cardioprotection by showing a transient increase in their levels during remote ischemic preconditioning (RIPC) phase. The transient increase in reactive oxygen species levels during remote preconditioning phase may take place either through activation of KATP channels or through increased nitric oxide (NO) production. A transient increase in reactive oxygen species during preconditioning may also increase the expression of heat shock proteins (HSP), the level of antioxidant enzymes and decrease the expression of inflammatory genes (Egr-1) during ischemia-reperfusion phase to confer cardioprotection. The present review describes the role of redox signaling in RIPC-induced cardioprotective effect with possible mechanisms.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2017.05.033</identifier><identifier>PMID: 28526338</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Antioxidant ; Coronary Vessels - physiology ; Coronary Vessels - physiopathology ; Heart ; Heat shock proteins ; Humans ; Ischemic Preconditioning ; Myocardium - cytology ; Myocardium - metabolism ; Myocardium - pathology ; Oxidation-Reduction ; Reactive Oxygen Species - metabolism ; Redox signaling ; Remote preconditioning ; Signal Transduction</subject><ispartof>European journal of pharmacology, 2017-08, Vol.809, p.151-155</ispartof><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3</citedby><cites>FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28526338$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>singh, Lovedeep</creatorcontrib><creatorcontrib>Randhawa, Puneet Kaur</creatorcontrib><creatorcontrib>Singh, Nirmal</creatorcontrib><creatorcontrib>Jaggi, Amteshwar Singh</creatorcontrib><title>Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Reactive oxygen species are the reactive molecules that are derived from molecular oxygen and play an important role as redox signaling molecules to confer cardioprotection. Various scientists have demonstrated the key role of redox signaling in cardioprotection by showing a transient increase in their levels during remote ischemic preconditioning (RIPC) phase. The transient increase in reactive oxygen species levels during remote preconditioning phase may take place either through activation of KATP channels or through increased nitric oxide (NO) production. A transient increase in reactive oxygen species during preconditioning may also increase the expression of heat shock proteins (HSP), the level of antioxidant enzymes and decrease the expression of inflammatory genes (Egr-1) during ischemia-reperfusion phase to confer cardioprotection. The present review describes the role of redox signaling in RIPC-induced cardioprotective effect with possible mechanisms.</description><subject>Animals</subject><subject>Antioxidant</subject><subject>Coronary Vessels - physiology</subject><subject>Coronary Vessels - physiopathology</subject><subject>Heart</subject><subject>Heat shock proteins</subject><subject>Humans</subject><subject>Ischemic Preconditioning</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Oxidation-Reduction</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Redox signaling</subject><subject>Remote preconditioning</subject><subject>Signal Transduction</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kMtKxDAUhoMoOl7eQCRLN60nSdM2LgQRbyAIouuQSU6dDNN0TDqDvr0ZRl26Oovz_efyEXLKoGTA6ot5ifPlzMSSA2tKkCUIsUMmrG1UAQ3ju2QCwKqCK6UOyGFKcwCQist9csBbyWsh2gnBF3TDJ03-PZiFD-_UBxqxH0akPtkZ9t7SZUQ7BOdHP4SMFD64lUVHrYnOD8uYYbvpXdLbtXcYLCZqgqM92pkJPvXpmOx1ZpHw5Kcekbe729ebh-Lp-f7x5vqpsKLmY6GUdMzITliDhvHKOMOlrJlVnUDW1HXluhZVXVVT10xROGx5wzveQC1Q4lQckfPt3HzUxwrTqPv8BS4WJuCwSpopgFYI4Cyj1Ra1cUgpYqeX0fcmfmkGeiNYz_VWsN4I1iB1FpxjZz8bVtMe3V_o12gGrrYA5j_XHqNO1m-cOJ81jtoN_v8N30EnkGw</recordid><startdate>20170815</startdate><enddate>20170815</enddate><creator>singh, Lovedeep</creator><creator>Randhawa, Puneet Kaur</creator><creator>Singh, Nirmal</creator><creator>Jaggi, Amteshwar Singh</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170815</creationdate><title>Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms</title><author>singh, Lovedeep ; Randhawa, Puneet Kaur ; Singh, Nirmal ; Jaggi, Amteshwar Singh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Antioxidant</topic><topic>Coronary Vessels - physiology</topic><topic>Coronary Vessels - physiopathology</topic><topic>Heart</topic><topic>Heat shock proteins</topic><topic>Humans</topic><topic>Ischemic Preconditioning</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Oxidation-Reduction</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Redox signaling</topic><topic>Remote preconditioning</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>singh, Lovedeep</creatorcontrib><creatorcontrib>Randhawa, Puneet Kaur</creatorcontrib><creatorcontrib>Singh, Nirmal</creatorcontrib><creatorcontrib>Jaggi, Amteshwar Singh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>singh, Lovedeep</au><au>Randhawa, Puneet Kaur</au><au>Singh, Nirmal</au><au>Jaggi, Amteshwar Singh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2017-08-15</date><risdate>2017</risdate><volume>809</volume><spage>151</spage><epage>155</epage><pages>151-155</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Reactive oxygen species are the reactive molecules that are derived from molecular oxygen and play an important role as redox signaling molecules to confer cardioprotection. Various scientists have demonstrated the key role of redox signaling in cardioprotection by showing a transient increase in their levels during remote ischemic preconditioning (RIPC) phase. The transient increase in reactive oxygen species levels during remote preconditioning phase may take place either through activation of KATP channels or through increased nitric oxide (NO) production. A transient increase in reactive oxygen species during preconditioning may also increase the expression of heat shock proteins (HSP), the level of antioxidant enzymes and decrease the expression of inflammatory genes (Egr-1) during ischemia-reperfusion phase to confer cardioprotection. The present review describes the role of redox signaling in RIPC-induced cardioprotective effect with possible mechanisms.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28526338</pmid><doi>10.1016/j.ejphar.2017.05.033</doi><tpages>5</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0014-2999
ispartof European journal of pharmacology, 2017-08, Vol.809, p.151-155
issn 0014-2999
1879-0712
language eng
recordid cdi_proquest_miscellaneous_1900833021
source ScienceDirect Freedom Collection 2022-2024
subjects Animals
Antioxidant
Coronary Vessels - physiology
Coronary Vessels - physiopathology
Heart
Heat shock proteins
Humans
Ischemic Preconditioning
Myocardium - cytology
Myocardium - metabolism
Myocardium - pathology
Oxidation-Reduction
Reactive Oxygen Species - metabolism
Redox signaling
Remote preconditioning
Signal Transduction
title Redox signaling in remote ischemic preconditioning-induced cardioprotection: Evidences and mechanisms
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T15%3A08%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Redox%20signaling%20in%20remote%20ischemic%20preconditioning-induced%20cardioprotection:%20Evidences%20and%20mechanisms&rft.jtitle=European%20journal%20of%20pharmacology&rft.au=singh,%20Lovedeep&rft.date=2017-08-15&rft.volume=809&rft.spage=151&rft.epage=155&rft.pages=151-155&rft.issn=0014-2999&rft.eissn=1879-0712&rft_id=info:doi/10.1016/j.ejphar.2017.05.033&rft_dat=%3Cproquest_cross%3E1900833021%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c362t-995d1a5f3caea124ada25561c9f3e17664df8e9644bd7be3de8272f27063e5eb3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1900833021&rft_id=info:pmid/28526338&rfr_iscdi=true