The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection-evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology.
The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection-evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology.
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DOI：
10.1007/s00395-018-0704-z
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发表时间：
2018-10-11
影响因子：
9.5
通讯作者：
Yellon DM
中科院分区：
文献类型：
--
作者：
Davidson SM;Arjun S;Basalay MV;Bell RM;Bromage DI;Bøtker HE;Carr RD;Cunningham J;Ghosh AK;Heusch G;Ibanez B;Kleinbongard P;Lecour S;Maddock H;Ovize M;Walker M;Wiart M;Yellon DM
由于其再生能力差，心脏对收缩性心肌细胞的丧失特别敏感。在急性心肌梗死和随后的再灌注治疗期间发生的缺血和再灌注引起的损伤的冲击可以消灭超过10亿个心肌细胞。类似的细胞死亡程序可导致缺血性中风中神经元的不可逆损失。致死细胞损伤的类似途径可导致其他病理，例如由癌症治疗引起的左心室功能障碍和心力衰竭。因此，旨在保护心脏免受致命细胞损伤的策略有可能适用于所有三种病理。在第10届哈特心血管研究所研讨会上，研究人员研究了ST段抬高型心肌梗死（STEMI），缺血性卒中和其他导致心肌细胞损失的病理学之间的相似性，包括癌症治疗心脏毒性。他们检查了每种情况下远程缺血条件（RIC）的保护前景，并评估了细胞保护的僵局和新机会，RIC在临床环境中的未来前景将由大型ERIC-PPCI/CONDI 2研究的结果确定。与会者一致认为，前进的道路必须包括改进实验方法的措施，使其更好地反映临床情况，并明智地选择针对细胞死亡和损伤特定途径的治疗组合。
Due to its poor capacity for regeneration, the heart is particularly sensitive to the loss of contractile cardiomyocytes. The onslaught of damage caused by ischaemia and reperfusion, occurring during an acute myocardial infarction and the subsequent reperfusion therapy, can wipe out upwards of a billion cardiomyocytes. A similar program of cell death can cause the irreversible loss of neurons in ischaemic stroke. Similar pathways of lethal cell injury can contribute to other pathologies such as left ventricular dysfunction and heart failure caused by cancer therapy. Consequently, strategies designed to protect the heart from lethal cell injury have the potential to be applicable across all three pathologies. The investigators meeting at the 10th Hatter Cardiovascular Institute workshop examined the parallels between ST-segment elevation myocardial infarction (STEMI), ischaemic stroke, and other pathologies that cause the loss of cardiomyocytes including cancer therapeutic cardiotoxicity. They examined the prospects for protection by remote ischaemic conditioning (RIC) in each scenario, and evaluated impasses and novel opportunities for cellular protection, with the future landscape for RIC in the clinical setting to be determined by the outcome of the large ERIC-PPCI/CONDI2 study. It was agreed that the way forward must include measures to improve experimental methodologies, such that they better reflect the clinical scenario and to judiciously select combinations of therapies targeting specific pathways of cellular death and injury.
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影响因子：
9.5
作者：
Bell RM;Bøtker HE;Carr RD;Davidson SM;Downey JM;Dutka DP;Heusch G;Ibanez B;Macallister R;Stoppe C;Ovize M;Redington A;Walker JM;Yellon DM
通讯作者：
Yellon DM
影响因子：
6.7
作者：
Chauveau, Fabien;Cho, Tae-Hee;Wiart, Marlene
通讯作者：
Wiart, Marlene
影响因子：
9.5
作者：
Cabrera-Fuentes HA;Aragones J;Bernhagen J;Boening A;Boisvert WA;Bøtker HE;Bulluck H;Cook S;Di Lisa F;Engel FB;Engelmann B;Ferrazzi F;Ferdinandy P;Fong A;Fleming I;Gnaiger E;Hernández-Reséndiz S;Kalkhoran SB;Kim MH;Lecour S;Liehn EA;Marber MS;Mayr M;Miura T;Ong SB;Peter K;Sedding D;Singh MK;Suleiman MS;Schnittler HJ;Schulz R;Shim W;Tello D;Vogel CW;Walker M;Li QO;Yellon DM;Hausenloy DJ;Preissner KT
通讯作者：
Preissner KT
在P2Y（12）受体拮抗剂治疗的大鼠中施用的VX-765抑制CASPase-1抑制caspase-1，可长期降低心肌梗塞大小和心室功能的保存。
影响因子：
9.5
作者：
Audia JP;Yang XM;Crockett ES;Housley N;Haq EU;O'Donnell K;Cohen MV;Downey JM;Alvarez DF
通讯作者：
Alvarez DF
影响因子：
3.4
作者：
Davidson SM;Takov K;Yellon DM
通讯作者：
Yellon DM