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Miguel A. Perez-Pinzon

Researcher at University of Miami

Publications -  197
Citations -  8957

Miguel A. Perez-Pinzon is an academic researcher from University of Miami. The author has contributed to research in topics: Ischemia & Ischemic preconditioning. The author has an hindex of 52, co-authored 178 publications receiving 8189 citations. Previous affiliations of Miguel A. Perez-Pinzon include Stanford University & Uppsala University.

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Resveratrol pretreatment protects rat brain from cerebral ischemic damage via a sirtuin 1-uncoupling protein 2 pathway.

TL;DR: In vivo resveratrol pretreatment confers neuroprotection similar to IPC via the SIRT1-UCP2 pathway, and significantly increased the ADP/O ratio in hippocampal mitochondria reflecting enhanced ATP synthesis efficiency.
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Ischaemic conditioning and targeting reperfusion injury: a 30 year voyage of discovery.

TL;DR: An overview of the major topics discussed at this special meeting of leading pioneers in the field of cardioprotection to review and discuss the history of IPC, its evolution to IPost and RIC, myocardial reperfusion injury as a therapeutic target, and future targets and strategies for cardioprotsection is provided.
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Resveratrol Mimics Ischemic Preconditioning in the Brain

TL;DR: It is reported that resveratrol pretreatment mimics IPC via the SIRT1 pathway, and may provide a novel therapy against stroke or neurosurgical procedures.
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Rapid preconditioning protects rats against ischemic neuronal damage after 3 but not 7 days of reperfusion following global cerebral ischemia

TL;DR: It is demonstrated that neuroprotection against acute neuronal injury can be achieved by conditioning insults followed by only short (30 min) periods of reperfusion, and subsequent rescue of neuronal populations could be achieved with better understanding of the neuroprotective mechanisms involved in this rapid IPC model.
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εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

TL;DR: It is corroborated here that IPC and a sublethal dose of NMDA were neuroprotective, whereas blockade ofNMDA receptors during IPC diminished IPC-induced neuroprotection, and it was demonstrated that the εPKC isozyme played a key role in both I PC- and NMDA-induced tolerance.