Rapamycin confers preconditioning-like protection against ischemia-reperfusion injury in isolated mouse heart and cardiomyocytes.

@article{Khan2006RapamycinCP,
  title={Rapamycin confers preconditioning-like protection against ischemia-reperfusion injury in isolated mouse heart and cardiomyocytes.},
  author={Shakil Akhtar Khan and Fadi N. Salloum and Anindita Das and Lei Xi and George W Vetrovec and Rakesh C. Kukreja},
  journal={Journal of molecular and cellular cardiology},
  year={2006},
  volume={41 2},
  pages={
          256-64
        }
}
Rapamycin protects against myocardial ischemia-reperfusion injury through JAK2-STAT3 signaling pathway.
Inhibition of mammalian target of rapamycin protects against reperfusion injury in diabetic heart through STAT3 signaling
TLDR
STAT3 signaling plays critical role in reducing IS and attenuates cardiomyocyte death following reperfusion therapy with rapamycin in diabetic heart.
Cardiac mTOR protects the heart against ischemia-reperfusion injury.
TLDR
It is suggested that cardiac mTOR overexpression in the heart is sufficient to provide substantial cardioprotection against I/R injury and suppress the inflammatory response.
Isoflurane Preconditioning Decreases Myocardial Infarction in Rabbits via Up-regulation of Hypoxia Inducible Factor 1 That Is Mediated by Mammalian Target of Rapamycin
TLDR
The current results indicate that isoflurane-induced myocardial protection involves activation of the HIF-1 pathway that is mediated by the mammalian target of rapamycin.
Infarct size is increased in female post-MI rats treated with rapamycin.
TLDR
It is demonstrated that rapamycin-sensitive signalling events were implicated in scar formation and reactive fibrosis in post-MI female rats and directly contributed to the larger infarct and attenuation of the reactive fibrotic response, respectively.
The influence of rapamycin on the early cardioprotective effect of hypoxic preconditioning on cardiomyocytes
TLDR
Rapamycin, through inhibition of mTOR, reduces the elevated HIF-1α expression at an early stage of HPC, and attenuates the early cardioprotective effect of H PC.
The late phase of ischemic preconditioning induces a prosurvival genetic program that results in marked attenuation of apoptosis.
mTOR‐mediated calcium transients affect cardiac function in ex vivo ischemia–reperfusion injury
TLDR
Heartbeat‐specific mTOR located to the SR/mitochondria plays a vital role in EC coupling and cell survival in I/R injury, and GSK3‐β phosphorylation, a key factor in SR calcium mobilization, was decreased.
Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway
TLDR
It is concluded that Rapamycin has a cardioprotection effect by inducing autophagy in a concentration-dependent manner against apopotosis through PI3K/Akt signaling pathway during A/R in NRVM.
Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway
TLDR
It is concluded that Rapamycin has a cardioprotection effect by inducing autophagy in a concentration-dependent manner against apopotosis through PI3K/Akt signaling pathway during A/R in NRVM.
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It is concluded that IP with repetitive cycles of brief GI/R is able to reduce myocardial infarct size and intracellular enzyme leakage caused by a sustainedGI/R in the isolated perfused mouse heart.
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TLDR
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