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Pinós Tomàs Fuku Noriyuki Cámara Yolanda Arai Yasumichi Abe Yukiko Rodríguez-Romo Gabriel Garatachea Nuria Santos-Lozano Alejandro Miro-Casas Elisabet Ruiz-Meana Marisol Otaegui Imanol Murakami Haruka Miyachi Motohiko Garcia-Dorado David Hinohara Kunihiko Andreu Antoni L. Kimura Akinori Hirose Nobuyoshi Lucia Alejandro 《Age (Dordrecht, Netherlands)》2014,36(2):933-943
GeroScience - The rs1333049 (G/C) polymorphism located on chromosome 9p21.3 is a candidate to influence extreme longevity owing to its association with age-related diseases, notably coronary artery... 相似文献
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Ruiz-Meana M Inserte J Fernandez-Sanz C Hernando V Miro-Casas E Barba I Garcia-Dorado D 《Basic research in cardiology》2011,106(6):1259-1268
Mitochondrial permeability transition (MPT) is critical in cardiomyocyte death during reperfusion but it is not the only mechanism
responsible for cell injury. The objectives of the study is to investigate the role of the duration of myocardial ischemia
on mitochondrial integrity and cardiomyocyte death. Mitochondrial membrane potential (ΔΨm, JC-1) and MPT (calcein) were studied
in cardiomyocytes from wild-type and cyclophilin D (CyD) KO mice refractory to MPT, submitted to simulated ischemia and 10 min
reperfusion. Reperfusion after 15 min simulated ischemia induced a rapid recovery of ΔΨm, extreme cell shortening (contracture)
and mitochondrial calcein release, and CyD ablation did not affect these changes or cell death. However, when reperfusion
was performed after 25 min simulated ischemia, CyD ablation improved ΔΨm recovery and reduced calcein release and cell death
(57.8 ± 4.9% vs. 77.3 ± 4.8%, P < 0.01). In a Langendorff system, CyD ablation increased infarct size after 30 min of ischemia (61.3 ± 6.4% vs. 45.3 ± 4.0%,
P = 0.02) but reduced it when ischemia was prolonged to 60 min (52.8 ± 8.1% vs. 87.6 ± 3.7%, P < 0.01). NMR spectroscopy in rat hearts showed a rapid recovery of phosphocreatine after 30 min ischemia followed by a marked
decay associated with contracture and LDH release, that were preventable with contractile blockade but not with cyclosporine
A. In contrast, after 50 min ischemia, phosphocreatine recovery was impaired even with contractile blockade (65.2 ± 4% at
2 min), and cyclosporine A reduced contracture, LDH release and infarct size (52.1 ± 4.2% vs. 82.8 ± 3.6%, P < 0.01). In conclusion, the duration of ischemia critically determines the importance of MPT on reperfusion injury. Mechanisms
other than MPT may play an important role in cell death after less severe ischemia. 相似文献
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