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10.3233/CH-200934

http://scihub22266oqcxt.onion/10.3233/CH-200934
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32924998!ä!32924998

suck abstract from ncbi


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pmid32924998      Clin+Hemorheol+Microcirc 2021 ; 77 (1): 91-105
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  • Protective effect of inhibiting TRPM7 expression on hypoxia post-treatment H9C2 cardiomyocytes #MMPMID32924998
  • Yang J; Hu S; Huang L; Zhou J; Xiang H; Yang H; Cheng H; Tang Y
  • Clin Hemorheol Microcirc 2021[]; 77 (1): 91-105 PMID32924998show ga
  • BACKGROUND: Transient receptor potential channel 7 (TRPM7) plays an important role in maintaining intracellular ion concentration and osmotic pressure. OBJECTIVE: The purpose of this study was to investigate the role and mechanism of inhibiting the expression of TRPM7 in the treatment of distal myocardial ischemia. METHODS: H9C2 cells were treated with hypoxia post-treatment and reperfusion, respectively, detect the expression of HIF-1alpha and TRPM7, the concentration of Ca2+ and the degree of apoptosis in the H9C2 cells. The relevant miRNAs targeting TRPM7 were searched, the TRPM7 interference vectors were constructed, and the interference of different interference vectors on TRPM7 in H9C2 cells was detected. RESULTS: The results showed that hypoxia post-treatment treatment would lead to increased expression of miR-22-3p which directly targeting TRPM7, decreased expression of TRPM7, increased expression of HIF-alpha and increased intracellular Ca2+ concentration. While reperfusion can increase the expression of HIF-1alpha and TRPM7 in H9C2 cells and increase the degree of apoptosis. CONCLUSION: Knockdown of TRPM7 can significantly reduce reperfusion injury in H9C2 cells, reduce the degree of apoptosis, and the TRPM7 interference vector can inhibit the expression of TRPM7 and have a certain protective effect on the reperfusion injury of H9C2 cells.
  • |Cell Hypoxia/*physiology[MESH]
  • |Humans[MESH]
  • |Myocytes, Cardiac/*metabolism[MESH]
  • |Protein Serine-Threonine Kinases/*metabolism[MESH]
  • |TRPM Cation Channels/*metabolism[MESH]


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