Murry et al in 1986 discovered the intrinsic mechanism of profound protection called ischemic preconditioning. The complex cellular signaling cascades underlying this phenomenon remain controversial and are only partially understood. However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C(PKC). This leads to the translocation of PKC from the cytoplasm to the sarcolemma, where it stimulates the opening of the ATP-sensitive K+ channel, which confers resistance to ischemia. It is known that a range of different hypoglycemic agents that activate the same signaling cascades at various cellular levels can interfere with protection from ischemic preconditioning. This review examines the effects of several hypoglycemic agents on myocardial ischemic preconditioning in animal studies and clinical trials.
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机译:Retraction: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction. Dong‐Mei Wu Yong‐Jian Wang Xin‐Rui Han Xin Wen Lei Li Lan Xu Jun Lu and Yuan‐Lin Zheng. J Cell Mol Med. 2018; 22: 3058–3072 (https://doi.org/10.1111/jcmm.13557).