TY - JOUR
T1 - Intercellular Communication in the Heart
T2 - Therapeutic Opportunities for Cardiac Ischemia
AU - Martins-Marques, Tania
AU - Hausenloy, Derek J.
AU - Sluijter, Joost P.G.
AU - Leybaert, Luc
AU - Girao, Henrique
N1 - Funding Information:
This work was supported by the European Regional Development Fund (ERDF) through the Operational Program for Competitiveness Factors (COMPETE) (under the projects PAC ‘NETDIAMOND' POCI-01-0145-FEDER-016385; HealthyAging2020 CENTRO-01-0145-FEDER-000012-N2323; POCI-01-0145-FEDER-007440, CENTRO-01-0145-FEDER-032179, CENTRO-01-0145-FEDER-032414, POCI-01-0145-FEDER-022122, FCTUID/NEU/04539/2013, UID/NEU/04539/2019, UIDB/04539/2020, and UIDP/04539/2020). T.M.M. was supported by PD/BD/106043/2015 from Fundação para a Ciência e a Tecnologia (FCT). D.J.H. was supported by the British Heart Foundation ( CS/14/3/31002 ), the Duke-NUS Signature Research Programme funded by the Ministry of Health , Singapore Ministry of Health ’s National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSA-SI/0011/2017), Centre Grant and Collaborative Centre Grant scheme (NMRC/CGAug16C006). This article is based upon work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST ( European Cooperation in Science and Technology ). J.P.G.S. was supported by Horizon2020 ERC-2016-CoG EVICARE (725229) and by the PPP Allowance Research Project from Top Sector Life Sciences & Health to Hartstichting (No. 2018B014). L.L. was supported by grants from the Fund for Scientific Research Flanders, Belgium (grant nos. G.0527.18N and G.0407.20N) and from the Special Research Fund of Ghent University
Funding Information:
This work was supported by the European Regional Development Fund (ERDF) through the Operational Program for Competitiveness Factors (COMPETE) (under the projects PAC ?NETDIAMOND' POCI-01-0145-FEDER-016385; HealthyAging2020 CENTRO-01-0145-FEDER-000012-N2323; POCI-01-0145-FEDER-007440, CENTRO-01-0145-FEDER-032179, CENTRO-01-0145-FEDER-032414, POCI-01-0145-FEDER-022122, FCTUID/NEU/04539/2013, UID/NEU/04539/2019, UIDB/04539/2020, and UIDP/04539/2020). T.M.M. was supported by PD/BD/106043/2015 from Funda??o para a Ci?ncia e a Tecnologia (FCT). D.J.H. was supported by the British Heart Foundation (CS/14/3/31002), the Duke-NUS Signature Research Programme funded by the Ministry of Health, Singapore Ministry of Health's National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSA-SI/0011/2017), Centre Grant and Collaborative Centre Grant scheme (NMRC/CGAug16C006). This article is based upon work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). J.P.G.S. was supported by Horizon2020 ERC-2016-CoG EVICARE (725229) and by the PPP Allowance Research Project from Top Sector Life Sciences & Health to Hartstichting (No. 2018B014). L.L. was supported by grants from the Fund for Scientific Research Flanders, Belgium (grant nos. G.0527.18N and G.0407.20N) and from the Special Research Fund of Ghent University
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2021/3
Y1 - 2021/3
N2 - The maintenance of tissue, organ, and organism homeostasis relies on an intricate network of players and mechanisms that assist in the different forms of cell–cell communication. Myocardial infarction, following heart ischemia and reperfusion, is associated with profound changes in key processes of intercellular communication, involving gap junctions, extracellular vesicles, and tunneling nanotubes, some of which have been implicated in communication defects associated with cardiac injury, namely arrhythmogenesis and progression into heart failure. Therefore, intercellular communication players have emerged as attractive powerful therapeutic targets aimed at preserving a fine-tuned crosstalk between the different cardiac cells in order to prevent or repair some of harmful consequences of heart ischemia and reperfusion, re-establishing myocardial function.
AB - The maintenance of tissue, organ, and organism homeostasis relies on an intricate network of players and mechanisms that assist in the different forms of cell–cell communication. Myocardial infarction, following heart ischemia and reperfusion, is associated with profound changes in key processes of intercellular communication, involving gap junctions, extracellular vesicles, and tunneling nanotubes, some of which have been implicated in communication defects associated with cardiac injury, namely arrhythmogenesis and progression into heart failure. Therefore, intercellular communication players have emerged as attractive powerful therapeutic targets aimed at preserving a fine-tuned crosstalk between the different cardiac cells in order to prevent or repair some of harmful consequences of heart ischemia and reperfusion, re-establishing myocardial function.
KW - acute myocardial infarction
KW - cardioprotection
KW - extracellular vesicles
KW - gap junctions
KW - intercellular communication
KW - remote ischemic conditioning
UR - http://www.scopus.com/inward/record.url?scp=85094806502&partnerID=8YFLogxK
U2 - 10.1016/j.molmed.2020.10.002
DO - 10.1016/j.molmed.2020.10.002
M3 - Review article
AN - SCOPUS:85094806502
SN - 1471-4914
VL - 27
SP - 248
EP - 262
JO - Trends in molecular medicine
JF - Trends in molecular medicine
IS - 3
ER -