TY - JOUR
T1 - Fondation Leducq Transatlantic Network of Excellence Targeting Mitochondria to Treat Heart Disease
AU - Murphy, Elizabeth
AU - Bernardi, Paolo
AU - Cohen, Michael
AU - Di Lisa, Fabio
AU - Forte, Michael
AU - Molkentin, Jeffery D.
AU - Ovize, Michel
N1 - Funding Information:
We acknowledge funding from Foundation Leducq.
PY - 2019/4/26
Y1 - 2019/4/26
N2 - Cell death is a major cause of cardiovascular disease, including myocardial infarction (MI) and heart failure (HF). Despite the progress made during the past 2 decades, acute MI and HF remain major causes of death worldwide. Although mitochondria play a fundamental role in heart physiology and metabolism, they are also key participants in underlying myocyte death after MI by opening of the mitochondrial permeability transition pore (PTP). The PTP, in which an inner membrane channel opens in response to increased matrix Ca2+ and reactive oxygen species (ROS), appears to be a universal mediator of regulated necrosis, and both Ca2+ and ROS are known to become dysregulated during MI and HF. Therefore, small molecule inhibitors of PTP are promising targets for the treatment of cardiovascular disease.
AB - Cell death is a major cause of cardiovascular disease, including myocardial infarction (MI) and heart failure (HF). Despite the progress made during the past 2 decades, acute MI and HF remain major causes of death worldwide. Although mitochondria play a fundamental role in heart physiology and metabolism, they are also key participants in underlying myocyte death after MI by opening of the mitochondrial permeability transition pore (PTP). The PTP, in which an inner membrane channel opens in response to increased matrix Ca2+ and reactive oxygen species (ROS), appears to be a universal mediator of regulated necrosis, and both Ca2+ and ROS are known to become dysregulated during MI and HF. Therefore, small molecule inhibitors of PTP are promising targets for the treatment of cardiovascular disease.
KW - cyclophilin D
KW - heart failure
KW - mitochondrial permeability transition pore
KW - phosphorylation
KW - reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=85065337175&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85065337175&partnerID=8YFLogxK
U2 - 10.1161/CIRCRESAHA.119.314893
DO - 10.1161/CIRCRESAHA.119.314893
M3 - Article
C2 - 31021720
AN - SCOPUS:85065337175
VL - 124
SP - 1294
EP - 1296
JO - Circulation Research
JF - Circulation Research
SN - 0009-7330
IS - 9
ER -